Immunity Case Study

Time To Read

18–28 minutes

Date Last Modified

Meeting Adjani

Adjani Mohammud is a 28-year-old high school math teacher who uses she/her pronouns. She lives in Rochester, New York, where she teaches algebra and loves her students. If you asked her students to describe her, they’d probably say ‘she’s the peanut butter teacher.’ Why? Because Adjani has eaten peanut butter sandwiches for lunch at least three times a week for her entire life. She keeps a jar of Skippy peanut butter in her desk drawer at school. Peanut butter cookies are her favorite dessert. She’s never had any problems with peanuts – until now.

But in the spring of 2023, Adjani’s life changed dramatically. She had been battling a progressive liver disease for several years, and by April 2023, her liver was failing. Her doctors told her the truth: without a liver transplant, she wouldn’t survive much longer.

Understanding Organ Transplantation

Adjani sits in Dr. Gordon’s transplant surgery office, trying to absorb what they’re telling her.

Dr. Gordon: “Adjani, your liver function tests show that your liver is no longer able to perform the tasks your body needs. We need to add you to the transplant waiting list.”

Adjani: “How long will I have to wait? And how do you even find a matching liver?”

Dr. Gordon: “Let me explain how the system works. In the United States, an organization called UNOS – the United Network for Organ Sharing – manages all organ transplants. When someone dies and their family agrees to donate their organs, UNOS uses a computer system to match those organs with patients on the waiting list.”

Adjani: “What makes a good match?”

The Science of Organ Matching

Dr. Gordon: “Great question. Organ matching is complex because your immune system is designed to attack anything it sees as ‘foreign’ or ‘not-self.’ Let me explain the key factors we consider.”

Blood Type Matching:

Just like blood transfusions, organs must be ABO compatible. Your blood type is O-positive, which is actually the most common blood type. You can receive organs from O-positive or O-negative donors.

Infographic detailing ABO blood types, showing antigens present on erythrocytes, antibodies in plasma, and compatibility for donation and reception across blood types A, B, AB, and O.

HLA Matching – The Major Histocompatibility Complex:

Dr. Gordon: “This is where it gets really interesting. Every cell in your body displays proteins on its surface called MHC proteins – that stands for Major Histocompatibility Complex. In humans, we call these HLA proteins – Human Leukocyte Antigens. Think of them like a molecular barcode that identifies cells as ‘you.’”

Diagram of human chromosome 6p21 showing the HLA region, featuring a representation of the chromosome's structure, labeled sections for HLA genes, and annotations for various gene locations.

Adjani: “How does my body know which proteins to make?”

Dr. Gordon: “Your HLA proteins are determined by your genes. You inherit three HLA genes from your mother and three from your father. These genes are located on chromosome 6, and they’re incredibly diverse – there are thousands of possible variations. This is why siblings have the best chance of matching, and why finding an unrelated donor match is so difficult.”

The Three Main HLA Types We Test:

  • HLA-A: One of the most variable HLA genes
  • HLA-B: Another highly variable gene
  • HLA-DR: Critical for immune recognition

Dr. Gordon: “We’ll type your HLA to help find the best match. But here’s something important to understand: there are two classes of MHC proteins, and they do different jobs.”

MHC Class I Proteins: Found on every nucleated cell in your body. They display pieces of proteins that the cell has made internally. CD8+ T cells – also called cytotoxic T cells – patrol your body looking at these MHC I proteins. If a cell is infected with a virus and displays viral proteins on its MHC I, the CD8+ T cell will kill that infected cell.

MHC Class II Proteins: Found only on specialized immune cells called antigen-presenting cells – this includes dendritic cells, macrophages, and B cells. These proteins display pieces of proteins that the cell has engulfed from outside. CD4+ T cells – also called helper T cells – monitor MHC II proteins and coordinate the immune response.

Diagram illustrating MHC Class I and Class II pathways for antigen processing and presentation in T cells. Includes steps for antigen uptake, processing, peptide-MHC association, and surface expression for CD8 and CD4 T cells.

Adjani: “So if I get someone else’s liver, my immune system will see those different HLA proteins and attack it?”

Dr. Gordon: “Exactly. That’s called rejection, and it’s why you’ll need to take immunosuppressive medications for the rest of your life. These drugs prevent your T cells from attacking the donated liver.”

On the Waiting List

On May 15, 2023, Adjani is officially added to the UNOS transplant waiting list. Her HLA typing results come back:

PatientHLA-AHLA-BHLA-DRB1
Adjani MohammudA2, A19B12, –DRB1*07, DRB1*13

Adjani’s doctors tell her that the wait for a liver could be months or even years. Her disease severity score places her in the moderate-urgency category.

The Call

On June 8, 2023 – just 24 days after being listed – Adjani receives the call. A liver is available. A 15-year-old boy named David Chen from Syracuse, New York (about 80 miles away) has been in a tragic car accident. When doctors determined that David could not survive his injuries, they asked his parents about organ donation.

David’s parents, devastated by their loss, knew that David had registered as an organ donor when he got his learner’s permit. Through their tears, they agreed to donate David’s organs. Medical records showed that David was healthy, active, and had plans to become a doctor someday. He had two notable medical conditions: asthma (well-controlled with medication) and a severe, documented peanut allergy with a history of anaphylaxis.

David’s medical records documented multiple emergency room visits for peanut exposure, including one incident at age 8 where he accidentally ate a cookie containing peanut butter and went into anaphylactic shock. David always carried two EpiPens. His father and maternal grandmother also had documented peanut allergies – it clearly ran in the family.

The HLA Match

UNOS analyzes David’s HLA type and compares it to patients on the waiting list. David’s organs will go to four different recipients. Let’s look at how well each recipient matches David’s HLA type:

RecipientOrganHLA-AHLA-BHLA-DRB1Match Quality
David (Donor)A1, A24B8, B44DRB1*03, DRB1*13
Adjani MohammudLiverA2, A19B12, –DRB1*07, DRB1*131 of 6 match (DRB1*13)
Maria RodriguezKidneyA1, A24B8, B44DRB1*03, DRB1*045 of 6 match
James PattersonHeartA1, A24B8, B44DRB1*03, DRB1*075 of 6 match
Robert WilliamsKidneyA3, A11B7, B35DRB1*01, DRB1*150 of 6 match

Notice that Robert Williams has the worst HLA match – he shares zero antigens with David. Adjani shares only one antigen (DRB1*13) with David. This means Adjani’s immune system will see David’s liver as very ‘foreign,’ and the risk of rejection is high. However, liver transplants are somewhat forgiving compared to kidney transplants – the liver has some immunological privilege because of its unique regenerative capacity and dual blood supply.

Understanding David’s Peanut Allergy

Before we continue with the transplant story, let’s understand what was happening in David’s immune system when he had allergic reactions to peanuts.

The Allergic Response – A Type I Hypersensitivity Reaction:

Peanut allergy is what we call an IgE-mediated, mast cell-dependent, immediate hypersensitivity reaction. Let’s break down what that means.

Step 1 – Sensitization (The First Exposure):

The first time David ate peanuts as a young child, his immune system mistakenly identified peanut proteins as dangerous invaders. Here’s what happened:

Diagram illustrating the immune response to allergens, highlighting the roles of dendritic cells, naive T cells, TH2 cells, and mast cells in allergen-specific IgE production and allergic reactions.
  • Dendritic cells (antigen-presenting cells) in his intestinal lining engulfed peanut proteins
  • These dendritic cells traveled to lymph nodes and displayed peanut protein fragments on their MHC Class II proteins
  • CD4+ T helper cells recognized the peanut proteins and became activated
  • These T helper cells differentiated into a specific type called Th2 cells
  • Th2 cells released cytokines (chemical messengers) including IL-4, IL-5, and IL-13
  • These cytokines signaled B cells to start producing IgE antibodies specific to peanut proteins

What are cytokines? Cytokines are small proteins that cells use to communicate with each other. They’re like text messages between immune cells. Different cytokines send different messages – some tell cells to divide, some tell cells to move to a specific location, and some tell cells to activate or calm down. T cells, macrophages, and many other immune cells produce cytokines.

Interleukin-2 (IL-2) is a particularly important cytokine. IL-2 is produced by activated T cells and tells other T cells to multiply and become more active. It’s essential for mounting an immune response. This is important because one of the immunosuppressive drugs we’ll discuss – cyclosporine – works by preventing IL-2 production.

Infographic illustrating lymphocyte subsets, their second-order cytokines, corresponding effector cells, and immune responses, including antibody production, mucosal activities, and T cell responses.

Understanding Antibodies:

Let’s pause to understand antibodies. Antibodies are Y-shaped proteins produced by B cells (and their descendants, plasma cells). There are five main types:

  • IgG: Most common antibody in blood, provides long-term immunity, can cross the placenta
  • IgM: First antibody produced in response to infection, very large
  • IgA: Found in mucus, saliva, tears, breast milk – protects mucosal surfaces
  • IgE: The allergy antibody – binds to mast cells and basophils
  • IgD: Found on B cell surfaces, helps activate B cells
Illustration of five types of antibodies: IgM, IgD, IgG, IgA, and IgE, showing their distinct structures and colors.

IgE – The Allergy Antibody:

IgE is special. Unlike other antibodies that float in the blood, IgE antibodies attach themselves to the surface of mast cells and basophils. These cells are loaded with granules containing powerful inflammatory chemicals. Once IgE antibodies coat these cells, they sit there waiting – sometimes for years – for the allergen to appear again.

Mast Cells and Basophils:

Mast cells are tissue-resident cells found throughout the body, especially in skin, lungs, and the lining of the digestive tract. They’re packed with granules containing histamine, heparin, proteases, and other inflammatory mediators.

Basophils are white blood cells that circulate in the blood. They’re similar to mast cells and also contain granules with inflammatory chemicals. Both cell types have IgE receptors on their surface.

Step 2 – Re-exposure and Degranulation:

The second time David ate peanuts, the allergic reaction happened:

  • Peanut proteins entered David’s body
  • The peanut proteins bound to the IgE antibodies sitting on mast cells and basophils
  • When multiple IgE antibodies on the same cell bind to peanut proteins, they cross-link together
  • This cross-linking triggers the cell to degranulate – the granules fuse with the cell membrane and dump their contents outside the cell
  • This happens within seconds to minutes – that’s why we call it an ‘immediate’ hypersensitivity reaction
Diagram illustrating the novel pathway of IgE-mediated drug allergy, showing the processes of sensitization and re-exposure, and the role of various immune cells like dendritic cells, T cells, B cells, and mast cells.

What Gets Released During Degranulation:

SubstanceSourceEffects
HistamineMast cells, basophilsVasodilation, increased vascular permeability, smooth muscle contraction, itching
HeparinMast cellsAnticoagulant, prevents blood clotting
Tryptase/ChymaseMast cellsProteases that activate complement, degrade proteins
Leukotrienes (LTC4, LTD4, LTE4)Mast cells, basophilsProlonged smooth muscle contraction, increased vascular permeability
ProstaglandinsMast cellsVasodilation, bronchoconstriction, pain
Platelet-activating factorMast cells, basophilsPlatelet activation, bronchoconstriction
Cytokines (TNF-α, IL-4, IL-5)Mast cellsRecruit more inflammatory cells, amplify response

The Clinical Symptoms:

These chemical mediators cause the symptoms of an allergic reaction:

  • Histamine causes: itching, hives, swelling, runny nose, watery eyes
  • Leukotrienes cause: airway constriction (wheezing, difficulty breathing)
  • Vasodilation and increased permeability cause: blood pressure drop, fluid leaking from vessels (angioedema)
  • In severe cases (anaphylaxis): life-threatening airway swelling and cardiovascular collapse

The Transplant Surgery

On June 9, 2023, Adjani undergoes liver transplant surgery at Strong Memorial Hospital in Rochester. The surgery lasts eight hours. Surgeons remove Adjani’s diseased liver and replace it with David’s healthy liver.

During the surgery and immediately after, Adjani receives aggressive immunosuppressive therapy. The goal is to prevent her T cells from recognizing David’s liver cells as foreign and mounting an attack.

Understanding Immunosuppressive Medications

The next day, Dr. Gordon explains Adjani’s medication regimen.

Adjani: “Why do I need so many different medications?”

Dr. Gordon: “Each medication attacks a different part of the immune response. Think of it like a multi-pronged defense strategy. Let me explain each one.”

The Immunosuppressive Regimen

MedicationMechanismDuration
Muromonab-CD3 (OKT3)Monoclonal antibody that binds to CD3 on T cells, forces apoptosis (cell death) of CD4+ and CD8+ T cells7 days (induction only)
Cyclosporine ABlocks calcineurin, prevents IL-2 production, stops T cell activation and proliferationLifelong
Prednisone (corticosteroid)Suppresses cytokine release, reduces inflammation, stabilizes cell membranes14 days tapered, then maintenance dose

Dr. Gordon: “Let me explain why each medication is critical.”

Muromonab-CD3 (OKT3) – The Nuclear Option:

This is a monoclonal antibody – a lab-made antibody designed to bind to a specific target. OKT3 binds to CD3, a protein found on all T cells. When OKT3 binds to CD3, it triggers the T cell to undergo apoptosis – programmed cell death. This dramatically reduces the number of T cells in your body for about a week, giving the transplanted liver time to settle in without being attacked.

Why target CD4+ T cells specifically? CD4+ T helper cells are the coordinators of the immune response. They’re the generals giving orders. If you eliminate the generals, the army can’t organize an attack. CD4+ T cells are essential for both:

  • Activating CD8+ cytotoxic T cells (which would directly kill liver cells)
  • Activating B cells to produce antibodies (which would lead to antibody-mediated rejection)

Without CD4+ T cells, the immune system cannot mount an effective attack on the transplanted organ. However, this also leaves Adjani very vulnerable to infections for the first week.

Cyclosporine A – Blocking the Activation Signal:

Illustration of the mechanism of action of Cyclosporine A (CsA) in T cells, showing the activation of T-cell receptors, calcium signaling, and subsequent IL-2 release.

Cyclosporine works differently. It doesn’t kill T cells – it prevents them from becoming activated. Here’s how:

  • When a T cell recognizes an antigen on MHC, it normally produces IL-2 (interleukin-2)
  • IL-2 is a growth signal – it tells the T cell to divide and multiply into an army of identical cells
  • Cyclosporine blocks an enzyme called calcineurin, which is required for IL-2 gene transcription
  • Without IL-2, T cells can’t proliferate, and the immune response stalls

Adjani will take cyclosporine for the rest of her life. This keeps her immune system in a state of controlled suppression – strong enough to fight infections, but too weak to reject the transplanted liver.

Corticosteroids (Prednisone) – The Anti-Inflammatory:

Corticosteroids are powerful anti-inflammatory drugs that work in multiple ways:

  • Suppress cytokine production (reduce IL-1, IL-2, IL-6, TNF-α, and many others)
  • Reduce the number of circulating lymphocytes
  • Stabilize cell membranes and reduce vascular permeability

Understanding Inflammation

Adjani: “You keep mentioning inflammation. What exactly is that?”

Dr. Gordon: “Inflammation is one of the body’s most important defense mechanisms. It’s what happens when your immune system responds to injury or infection.”

The Cardinal Signs of Inflammation (described by the ancient Romans):

  • Rubor (redness): Increased blood flow to the area
  • Calor (heat): Warmth from increased blood flow and metabolic activity
  • Tumor (swelling): Fluid accumulation from increased vascular permeability
  • Dolor (pain): Pressure on nerve endings and release of pain-inducing chemicals
  • Functio laesa (loss of function): The injured area cannot work properly

Benefits of Inflammation:

  • Delivers immune cells to the site of infection or injury
  • Increases vascular permeability so antibodies and complement proteins can reach tissues
  • Activates the clotting system to wall off infections
  • Induces pain, which protects the area from further damage
  • Initiates tissue repair and healing

Dr. Gordon: “But in the case of organ transplant, we want to suppress inflammation. Why? Because inflammation is part of the rejection process. When your T cells recognize David’s liver as foreign, they release inflammatory cytokines that recruit more immune cells, damage tissue, and ultimately destroy the transplanted organ. Corticosteroids prevent this by suppressing the inflammatory cascade.”

Recovery and Going Home

The transplant is successful! Within days, David’s liver is working perfectly in Adjani’s body. Her liver function tests normalize, and her energy returns. After two weeks in the hospital, Adjani goes home to continue her recovery.

She’s taking cyclosporine twice daily and a low dose of prednisone. Her doctors monitor her closely with weekly blood tests to check liver function and ensure proper cyclosporine levels. She’s also taking antiviral medications to prevent opportunistic infections while her immune system is suppressed.

Adjani writes a heartfelt letter to David’s family (sent through UNOS to maintain anonymity) thanking them for the gift of life. She dreams of returning to her classroom in the fall.

But something unexpected is about to happen – something that will forever change Adjani’s relationship with her favorite food.

Part 2: The Mysterious Allergy

The First Incident – Ten Days Post-Transplant

On June 19, 2023 – just 10 days after her transplant – Adjani is feeling well enough to eat normally. She’s at home, and she’s craving comfort food. She makes herself a peanut butter and jelly sandwich, one of her lifelong favorites.

She takes a bite. It tastes as good as always. She takes another bite.

Within 20 minutes, Adjani notices something strange. Her skin starts to itch – first on her arms, then spreading to her neck and chest. She looks down and sees red, raised bumps appearing on her skin. Hives.

Adjani has never had hives before. She calls her transplant coordinator.

Transplant Coordinator: “It’s probably just a reaction to the medications. Take some Benadryl and see if it improves. If it gets worse or you have trouble breathing, go to the ER immediately.”

The Benadryl works. Within a few hours, the hives fade. Adjani doesn’t make the connection to the peanut butter – she assumes it’s related to her transplant medications or maybe something else she ate.

The Second Incident – Life-Threatening

On June 27, 2023 (18 days after transplant), Adjani decides to celebrate feeling better by baking peanut butter cookies – David’s grandmother’s recipe that she’s made hundreds of times. She mixes the dough, bakes the cookies, and eats two warm cookies fresh from the oven.

Diagram illustrating the process of allergens entering the gut, binding to IgE on mast cells, and activating them. The first part shows allergens binding to IgE and mast cells in a normal gut environment. The second part depicts the activation of mast cells leading to smooth muscle contraction and fluid outflow into the gut, resulting in inflammation and allergic reactions.

This time, the reaction is immediate and severe.

Within 15 minutes:

  • Hives erupt across Adjani’s entire body
  • Her lips and tongue swell dramatically
  • A raised, red rash spreads across her chest
  • Her throat feels tight – she can’t swallow properly
  • She’s wheezing and struggling to breathe
  • She feels dizzy and nauseated

Adjani’s husband immediately drives her to the emergency room. The ER doctors recognize the symptoms immediately: anaphylaxis – a life-threatening allergic reaction.

Emergency Treatment

The ER team acts fast:

  • Epinephrine injection (0.3 mg intramuscular) – counteracts the effects of histamine, reverses bronchoconstriction, raises blood pressure
  • IV diphenhydramine (Benadryl) – blocks histamine receptors
  • IV methylprednisolone (corticosteroid) – reduces inflammation, prevents biphasic reaction
  • Continuous monitoring of vital signs, oxygen saturation

Within 30 minutes, Adjani’s symptoms begin to improve. Her airway opens, her blood pressure stabilizes, and the hives start to fade. She’s kept for observation for six hours (anaphylaxis can sometimes have a second wave of symptoms 4-8 hours later called a biphasic reaction).

Before discharge, the ER doctor asks a critical question:

ER Doctor: “What did you eat before this happened?”

Adjani: “Peanut butter cookies. But I’ve eaten peanut butter my whole life. I’m not allergic to peanuts.”

ER Doctor: “You are now. This was a classic peanut anaphylaxis. You need to see an allergist immediately, and you need to avoid all peanuts until then.”

The Allergist Consultation

Three days later, Adjani sits in the office of Dr. Sarah Williams, an immunologist and allergist. Dr. Williams has already reviewed Adjani’s medical records and is very interested in the timing of this allergy.

Dr. Williams: “Adjani, I want to run some tests to confirm what I suspect. But first, let me ask: did anyone in your biological family have food allergies?”

Adjani: “No, never. And I’ve eaten peanuts my entire life without any problems.”

Dr. Williams: “I want to tell you something about your donor. David Chen had a severe, documented peanut allergy. His medical records show multiple anaphylactic reactions. His father and grandmother also had peanut allergies. I think what’s happened is extraordinary – I believe David’s liver has transferred his peanut allergy to you.”

The Testing

Test #1: Skin Prick Test

Dr. Williams performs a skin prick test. She places a tiny drop of peanut extract on Adjani’s forearm and uses a small lancet to prick the skin, allowing the extract to enter the top layer of skin.

Within minutes, a large, red, itchy wheal appears at the test site – about 8mm in diameter with surrounding redness (flare). This is a strongly positive reaction.

Why does the skin test work? Mast cells in the skin have IgE antibodies bound to their surface. When the peanut allergen enters the skin, it cross-links these IgE antibodies, triggering the mast cells to degranulate and release histamine. The histamine causes vasodilation (redness), increased vascular permeability (wheal formation), and itching.

Result: POSITIVE for peanut allergy

Test #2: Serum IgE Test (RAST)

Dr. Williams orders a blood test called a RadioAllergoSorbent Test (RAST) – now more commonly called an ImmunoCAP test. This test measures the amount of peanut-specific IgE antibodies floating in Adjani’s bloodstream.

The results come back negative – there are no detectable peanut-specific IgE antibodies in Adjani’s blood.

Adjani: “I don’t understand. The skin test was positive, but the blood test was negative? How can I be allergic if I don’t have IgE antibodies?”

Test #3: Basophil Activation Test

Dr. Williams: “This is the fascinating part. I want to do one more test – a basophil activation test. We’ll take some of your blood, mix it with peanut extract in the lab, and look at what happens to your basophils.”

The lab performs the test. They isolate basophils from Adjani’s blood and expose them to peanut allergen. Under the microscope, the technicians watch as the basophils degranulate – the granules fuse with the cell membrane and dump their contents. They can measure this by looking for activation markers that appear on the basophil surface during degranulation.

Result: POSITIVE – Adjani’s basophils degranulate in response to peanut allergen

The Explanation

Dr. Williams: “Here’s what I believe happened. David’s liver contained memory B cells that were already programmed to produce peanut-specific IgE antibodies. When you received his liver, those B cells came with it. They survived in your body because you’re taking immunosuppressive medications that prevent your immune system from killing them.”

Adjani: “So I have David’s B cells living in my body?”

Dr. Williams: “Exactly. The liver is a lymphoid organ – it contains immune cells, including B cells. David’s peanut-specific B cells migrated from his liver into your body. These cells don’t produce IgE constantly – they only produce it when stimulated by the allergen or when signaled by T cells. That’s why your blood IgE test was negative.”

Dr. Williams: “However, David’s B cells DID produce IgE locally. That IgE bound to mast cells in your tissues – especially in your skin and gastrointestinal tract. That’s why your skin test was positive – you have mast cells coated with peanut-specific IgE. And that’s why you had anaphylaxis when you ate peanuts.”

Adjani: “Will this go away? Or am I allergic to peanuts forever?”

Dr. Williams: “That’s uncertain. Documented cases of transferred allergies have shown different outcomes. Some people’s allergies persist for years. Others have seen the allergy gradually fade as the donor B cells die off. But as long as you’re on immunosuppressive medications, those donor B cells will likely survive. You’ll need to avoid peanuts completely and carry epinephrine at all times.”

Diagram of immune organs in the human body, labeling lymph nodes, lymph vessels, liver, Peyer's patches, spleen, thymus, and bone marrow.

The Other Recipients – A Scientific Mystery

Dr. Williams contacts the transplant coordinators for the other three recipients of David’s organs. She wants to know if they experienced similar reactions.

RecipientOrgan ReceivedPeanut Allergy Developed?
Adjani MohammudLiverYES – severe anaphylaxis
Maria RodriguezKidneyNO – continues eating peanuts
James PattersonHeartNO – continues eating peanuts
Robert WilliamsKidneyNO – continues eating peanuts

Adjani: “Why am I the only one? We all got David’s organs. We’re all on immunosuppressive drugs.”

Dr. Williams: “The liver is unique. It’s the largest lymphoid organ in the body after the spleen. It contains a huge population of immune cells – B cells, T cells, natural killer cells, Kupffer cells (specialized macrophages). When you received David’s liver, you received a significant portion of his immune system.”

Dr. Williams: “The heart and kidneys contain far fewer immune cells. Maria, James, and Robert received David’s organs, but they didn’t receive enough of his immune cells to transfer the allergy. You did.”

Living with a Transferred Allergy

Dr. Williams prescribes:

  • Two EpiPens (epinephrine auto-injectors) to carry at all times
  • Medical alert bracelet: “PEANUT ALLERGY – ANAPHYLAXIS RISK”
  • Strict avoidance of all peanuts and peanut-containing products
  • Instructions for reading food labels carefully
  • Plan for informing her school about the allergy

Adjani: “This is so strange. I loved peanut butter. It was comfort food for me. And now I have to avoid it completely because… because I have someone else’s immune cells?”

Dr. Williams: “I know it’s difficult. But think about it this way: David’s liver saved your life. His immune cells came along with that gift. In a sense, a small part of David continues to live on in you – both his liver cells and his immune cells.”

Adjani: “That’s actually kind of beautiful. I just wish the part that came with him wasn’t an allergy!”

Six Months Later

Adjani has adapted to life with a peanut allergy. She’s back teaching at the high school, but her students now call her ‘the almond butter teacher’ instead. She carries her EpiPens everywhere. She’s become an advocate for organ donation, sharing her story of how David’s gift saved her life.

She had her allergy tested again six months post-transplant. The skin prick test remains strongly positive. The basophil activation test remains positive. Her blood IgE test is still negative – suggesting that David’s memory B cells are still producing IgE locally in tissues, but not releasing it into her bloodstream in large quantities.

Dr. Williams tells her the allergy may persist as long as she takes immunosuppressive medications – possibly for life. But Adjani has made peace with it.

Adjani: “I’m alive. My liver works perfectly. I can teach, I can laugh, I can plan for the future. David and his family gave me that. If the price I pay is avoiding peanut butter, that’s more than fair. I carry a piece of David with me – literally – and I’ll honor his gift by living the best life I can.”

Adjani’s case has been documented in medical literature as one of the rare but fascinating examples of passive transfer of allergy through solid organ transplantation – a testament to the complex relationship between the immune system, genetics, and the organs that house our immune cells.

List of terms