- This destruction occurs through which primary Type II hypersensitivity mechanisms?
Answer: Opsonization leading to phagocytosis and activation of the classical complement pathway leading to intravascular lysis.
An acute ABO-incompatible transfusion reaction is a classic Type II hypersensitivity. The pre-formed anti-B IgM and IgG antibodies in the recipient's plasma bind to the B antigens on donor red blood cells. This binding leads to two main destructive pathways: (1) powerful activation of the classical complement cascade, resulting in the formation of the membrane attack complex (MAC) and intravascular hemolysis; and (2) opsonization of the erythrocytes, marking them for phagocytosis by macrophages in the spleen and liver (extravascular hemolysis). The other options incorrectly invoke mechanisms from Type III (B), Type IV (C), and Type I/IV (D) hypersensitivity.
- Which of the following hypersensitivity reactions is unique in that its effector phase is primarily initiated and executed by lymphocytes and phagocytes, without the direct involvement of antibodies as the principal mediators of tissue damage?
Answer: Type IV hypersensitivity
When you encounter questions about hypersensitivity reactions, focus on the key mediators driving tissue damage in each type. The four types of hypersensitivity differ fundamentally in their effector mechanisms and timing.
Type IV hypersensitivity stands apart as the only delayed-type reaction that operates independently of antibodies. Instead, it's driven entirely by T lymphocytes and activated macrophages. When sensitized T cells encounter their specific antigen, they release cytokines that recruit and activate macrophages, which then cause tissue damage through direct cellular mechanisms. Classic examples include contact dermatitis from poison ivy and tuberculin skin tests.
Option A (Type III) is incorrect because it depends heavily on immune complex formation between antibodies and antigens, which then deposit in tissues and trigger complement activation. Option B (Type I) is wrong since it's mediated by IgE antibodies bound to mast cells and basophils, causing immediate degranulation and histamine release. Option C (Type II) relies on antibodies that directly bind to cell surface antigens, leading to complement-mediated cell destruction or antibody-dependent cellular cytotoxicity.
The critical distinction is timing and mediators: Types I, II, and III are antibody-mediated and occur within minutes to hours, while Type IV is cell-mediated and develops over 24-72 hours as T cells mobilize inflammatory responses.
Remember this pattern: if a hypersensitivity question emphasizes lymphocyte-mediated responses without antibody involvement, think Type IV. This cellular immunity mechanism is fundamentally different from the humoral (antibody-based) responses characterizing the other three types.
- Both Goodpasture syndrome and post-streptococcal glomerulonephritis (PSGN) can present with acute renal failure due to glomerular inflammation. What is the key feature that distinguishes the pathogenesis of PSGN from that of Goodpasture syndrome?
Answer: In PSGN, the antigen is exogenous and forms circulating immune complexes, while in Goodpasture, the antigen is an endogenous component of the glomerular basement membrane.
When you encounter questions about glomerulonephritis, focus on the fundamental mechanism driving each disease: where the antigen comes from and how immune complexes form.
Post-streptococcal glomerulonephritis (PSGN) occurs when streptococcal antigens (exogenous, from outside the body) circulate in the bloodstream and form immune complexes with antibodies. These preformed circulating immune complexes then deposit in the glomeruli, triggering inflammation. Think of it as the kidney being an innocent bystander damaged by immune complexes formed elsewhere.
Goodpasture syndrome works completely differently. Here, antibodies directly attack the glomerular basement membrane (GBM) itself because they recognize an endogenous antigen (type IV collagen) as foreign. The immune complexes form in situ (right at the GBM), not in circulation. This is why Goodpasture can also affect lung basement membranes, which contain similar collagen.
Option A is wrong because both conditions involve IgG antibodies, not IgE. Option B incorrectly characterizes PSGN as T-cell mediated when it's actually antibody-mediated like Goodpasture. Option D focuses on complement pathways, but both diseases can activate complement through the classical pathway when immune complexes form.
The key distinction is antigen source and immune complex formation location: PSGN involves exogenous antigens forming circulating immune complexes that deposit secondarily, while Goodpasture involves endogenous antigens with immune complexes forming directly at the target tissue.
Study tip: Remember "PSGN = Posted complexes, Goodpasture = GBM attack" to distinguish circulating immune complex deposition from direct basement membrane targeting.
- The induration observed in a positive tuberculin skin test is a direct result of a local inflammatory response characteristic of a Type IV hypersensitivity. This response is orchestrated primarily by the secretion of specific cytokines from which cell type?
Answer: Antigen-specific Th1 cells secreting interferon-gamma (IFN-γ) to activate macrophages.
When you encounter questions about tuberculin skin tests, think about the four types of hypersensitivity reactions and which immune cells drive each one. The tuberculin test exemplifies Type IV (delayed-type) hypersensitivity, which is fundamentally different from the immediate allergic reactions most people know.
The induration you observe 48-72 hours after tuberculin injection results from a T-cell mediated response. Specifically, memory Th1 cells that previously encountered tuberculosis antigens recognize the injected tuberculin and become activated. These Th1 cells secrete interferon-gamma (IFN-γ), which is the key cytokine that activates local macrophages. The activated macrophages accumulate at the injection site, creating the characteristic firm, raised induration. This makes option C correct.
Option A describes a humoral immune response with antibody production, which characterizes Type II hypersensitivity, not the cell-mediated Type IV response seen in tuberculin tests. Option B represents Type I hypersensitivity (immediate allergic reactions) involving Th2 cells and IgE—this would cause immediate swelling and itching, not delayed induration. Option D also describes Type I hypersensitivity with mast cell degranulation, which again would produce immediate symptoms rather than the delayed, firm induration characteristic of tuberculin tests.
Remember this pattern: Type IV hypersensitivity always involves T-cells (specifically Th1), takes 24-72 hours to develop, and creates firm induration rather than soft swelling. The key cytokine is always IFN-γ activating macrophages.
- The pathogenesis of this patient's condition is characteristic of which hypersensitivity type?
Answer: Type II, involving autoantibodies against antigens intrinsic to the basement membrane.
When you encounter a case combining rapidly progressive glomerulonephritis with pulmonary symptoms and linear IgG deposits on immunofluorescence, you're looking at Goodpasture syndrome - a classic example of type II hypersensitivity.
The key diagnostic clue here is the linear pattern of IgG deposition along the glomerular basement membrane (GBM). This occurs because autoantibodies directly bind to specific antigens (primarily the α3 chain of type IV collagen) that are intrinsic components of both glomerular and alveolar basement membranes. This direct antibody-antigen binding creates the characteristic linear immunofluorescence pattern and explains why patients develop both kidney and lung involvement.
Answer D correctly identifies this as type II hypersensitivity, which involves antibodies directed against fixed tissue antigens, leading to complement activation and tissue damage.
Answer A is wrong because type I hypersensitivity involves IgE-mediated mast cell degranulation causing immediate allergic reactions, not autoimmune glomerulonephritis with linear deposits.
Answer B describes type III hypersensitivity, which involves circulating immune complexes that deposit in tissues. However, this creates a granular (not linear) immunofluorescence pattern, as seen in lupus nephritis or post-streptococcal glomerulonephritis.
Answer C refers to type IV hypersensitivity, which is T-cell mediated (like contact dermatitis or transplant rejection) and doesn't involve antibody deposition patterns on immunofluorescence.
Study tip: Remember the immunofluorescence patterns - linear deposits suggest antibodies against basement membrane antigens (type II), while granular deposits suggest immune complex deposition (type III). This distinction frequently appears on pathophysiology exams.
- The primary immunological event responsible for the patient's acute signs and symptoms is the binding of which components?
Answer: Pre-existing anti-A and anti-B IgM/IgG in the recipient's plasma to A and B antigens on the donor erythrocytes.
When you encounter a transfusion reaction scenario, focus on the timeline and the patient's blood type to identify which immunological mechanism is at play. This case involves an immediate reaction (within 30 minutes) with classic signs of acute hemolytic transfusion reaction: fever, flank pain, and hemoglobinuria (dark red urine from lysed red blood cells).
The correct answer is C because O-negative patients naturally possess pre-existing anti-A and anti-B antibodies in their plasma. These antibodies developed early in life through exposure to A and B antigens from environmental sources. When AB-positive blood (containing both A and B antigens) is transfused, these pre-existing IgM and IgG antibodies immediately bind to the foreign antigens on donor red blood cells, causing rapid hemolysis through complement activation and the classical pathway.
Option A is incorrect because IgE-mediated reactions require prior sensitization and typically cause anaphylactic symptoms, not hemolytic ones. Additionally, newly formed antibodies wouldn't appear within 30 minutes.
Option B is wrong because anti-Rh antibodies don't naturally occur in Rh-negative individuals—they only develop after exposure to Rh-positive blood through previous transfusion or pregnancy. Even if present, Rh incompatibility typically causes delayed reactions, not acute hemolysis.
Option D describes graft-versus-host disease, which involves donor T-cells attacking recipient tissues over weeks to months, not an acute 30-minute reaction.
Study tip: Remember that ABO incompatibility causes immediate, severe reactions because the antibodies are naturally occurring, while other blood group incompatibilities usually require prior sensitization and cause delayed reactions.
- What is the key immunological distinction between the hypersensitivity reactions experienced by these two patients?
Answer: The first patient's reaction targets antigens fixed on cell surfaces, while the second patient's reaction involves soluble antigen-antibody complexes.
The first patient has a Type II hypersensitivity reaction, where antibodies target antigens bound to a cell surface (in this case, penicillin-modified erythrocytes). The second patient has a Type III hypersensitivity reaction (serum sickness), where damage is caused by the deposition of soluble, circulating antigen-antibody complexes. This distinction—cell-bound vs. soluble antigen—is the fundamental difference between Type II and Type III reactions. Both are antibody-mediated, invalidating option B. Option C misidentifies the immunoglobulins. Option D incorrectly describes the primary mechanisms.
- The central role of immunoglobulin E (IgE) in Type I hypersensitivity is functionally distinct from the roles of IgG and IgM in Type II and III reactions. This distinction is primarily based on IgE's unique ability to:
Answer: bind to high-affinity Fc receptors (FcεRI) on mast cells and basophils in the absence of an antigen.
When you encounter questions about hypersensitivity reactions, focus on the unique mechanisms that distinguish each type, particularly how different antibody classes interact with immune cells.
IgE's defining characteristic is its ability to bind to high-affinity Fc epsilon receptors (FcεRI) on mast cells and basophils even before encountering an antigen. This pre-positioning is what makes Type I hypersensitivity so rapid and explosive. Once IgE is bound to these cells, subsequent exposure to the specific antigen causes cross-linking of the surface-bound IgE molecules, triggering immediate degranulation and release of inflammatory mediators like histamine. This mechanism is fundamentally different from Type II and III reactions, where antibodies must first encounter their targets before immune activation occurs.
Looking at the incorrect options: (A) is wrong because IgE actually has poor complement-activating ability compared to IgG and IgM - this is characteristic of Type II/III reactions, not Type I. (C) describes IgG, not IgE; IgE cannot cross the placenta due to its molecular structure and receptor binding properties. (D) also describes IgG function - IgE does not act as an opsonin for phagocytosis.
The key study point here is that IgE's pre-positioning on effector cells makes Type I reactions uniquely immediate, while Type II and III reactions depend on antibody-antigen immune complex formation first. Remember: IgE = immediate because it's already in position; IgG/IgM = delayed because they must find their targets first.
- The development of all four types of hypersensitivity requires an initial "sensitization" phase, followed by an "effector" phase upon subsequent exposure. Which of the following events occurs exclusively during the sensitization phase of a Type IV reaction, such as contact dermatitis to nickel?
Answer: Presentation of a hapten-carrier complex by Langerhans cells to naive T-lymphocytes in a regional lymph node, leading to their clonal expansion and differentiation into memory cells.
Type IV hypersensitivity reactions are T-cell mediated delayed responses that require two distinct phases. Understanding what happens exclusively during sensitization versus the effector phase is crucial for distinguishing these mechanisms.
During the sensitization phase of contact dermatitis, the immune system first encounters and processes the antigen. Answer B correctly describes this initial phase: Langerhans cells (specialized dendritic cells in the skin) capture the hapten-carrier complex and migrate to regional lymph nodes. There, they present the antigen to naive T-lymphocytes, triggering their activation, clonal expansion, and differentiation into memory T-cells. This creates the immunological "memory" that enables the dramatic response upon re-exposure.
Answer A describes the effector phase, not sensitization. The release of IFN-γ and macrophage recruitment happens during subsequent exposures when memory T-cells are reactivated and mount the inflammatory response that causes the clinical symptoms.
Answer C describes Type I hypersensitivity (immediate allergic reactions), where B-cells undergo isotype switching to produce IgE antibodies that bind to mast cells. This is entirely different from the T-cell mediated Type IV mechanism.
Answer D describes Type III hypersensitivity, involving immune complex formation and complement activation in blood vessels, which is unrelated to the cell-mediated contact dermatitis mechanism.
Study tip: For hypersensitivity questions, always identify the type first, then distinguish between sensitization (initial antigen processing and memory formation) and effector phases (the actual inflammatory response upon re-exposure). Type IV is always T-cell mediated, never involves antibodies.
- Which of the following pathophysiological events is least likely to be a component of this reaction?
Answer: Infiltration of affected tissue by antigen-specific CD4+ T-cells and macrophages peaking at 48 hours.
When you encounter a case of rapid-onset urticaria, angioedema, and bronchospasm after allergen exposure, you're looking at a classic Type I hypersensitivity reaction (anaphylaxis). The key insight is understanding the timeline: this is an immediate reaction occurring within minutes, not hours or days.
The correct answer is C because antigen-specific CD4+ T-cell and macrophage infiltration peaking at 48 hours describes a delayed-type hypersensitivity reaction (Type IV), which occurs over days, not minutes. This patient's symptoms are far too rapid for cellular immune responses that require time for chemotaxis, migration, and tissue infiltration.
Let's examine why the other options are integral to immediate hypersensitivity: Option A correctly describes degranulation of mast cells and basophils, which release preformed mediators like histamine (causing urticaria and vasodilation) and tryptase (a marker used clinically to confirm anaphylaxis). Option B identifies the triggering mechanism - multivalent allergens cross-linking surface-bound IgE antibodies, which initiates the cascade. Option D describes the secondary wave of newly synthesized inflammatory mediators like leukotrienes and prostaglandins, which sustain and amplify the reaction within minutes to hours.
For pathophysiology exams, remember that hypersensitivity reactions follow distinct timelines: Type I (immediate, minutes), Type II and III (hours), and Type IV (days). When you see rapid onset of systemic allergic symptoms, focus on IgE-mediated mechanisms involving mast cells and basophils, not delayed cellular responses.
- The mechanism responsible for this patient's thrombocytopenia is best categorized as which type of hypersensitivity?
Answer: Type II
When you encounter drug-induced thrombocytopenia with bleeding symptoms, focus on identifying the immune mechanism involved. The key clue here is "drug-dependent antibodies that bind to platelet surface glycoproteins only when quinine is present" - this describes a specific antibody-mediated reaction pattern.
This represents Type II hypersensitivity, making D correct. In Type II reactions, antibodies bind directly to cell surface antigens, leading to cell destruction. Here, quinine acts as a hapten - a small molecule that becomes immunogenic when bound to platelet glycoproteins. The resulting antibodies only recognize the quinine-platelet complex, explaining why they bind "only when quinine is present." Once bound, these antibodies trigger complement activation and platelet destruction, causing the severe thrombocytopenia (15,000/μL) and bleeding symptoms.
A (Type IV) is incorrect because this involves T-cell mediated delayed hypersensitivity, not antibodies. The presence of specific antibodies and acute onset rules this out.
B (Type I) is wrong because this describes IgE-mediated allergic reactions causing mast cell degranulation and anaphylaxis, not direct cell destruction by antibodies.
C (Type III) involves immune complex formation and deposition in tissues, typically causing vasculitis or nephritis. While antibodies are involved, they don't directly bind to target cells like platelets.
Remember: Drug-dependent antibodies that require the drug's presence to bind target cells are classic for Type II hypersensitivity. Watch for this pattern with heparin-induced thrombocytopenia and other drug-induced cytopenias on exams.
- In this previously sensitized child, what is the initial molecular event that triggers the rapid release of vasoactive amines?
Answer: Cross-linking of FcεRI-bound IgE on mast cells by peanut allergens.
This scenario describes a Type I hypersensitivity reaction. In a previously sensitized individual, mast cells and basophils are coated with allergen-specific IgE antibodies bound to high-affinity Fc receptors (FcεRI). Upon re-exposure, the allergen (peanut protein) cross-links these IgE molecules, triggering signal transduction and the immediate degranulation of the cell, releasing pre-formed mediators like histamine. Option C describes the initial sensitization phase, not the effector phase. Option B describes a Type II/III mechanism. Allergens do not directly bind to histamine receptors (Option D); histamine does.
- Which statement best explains this pattern of reactivity?
Answer: The first exposure induced sensitization of antigen-specific T-cells, which then mediated a delayed-type hypersensitivity reaction upon the second exposure.
When you encounter questions about delayed skin reactions after repeated exposure, you're dealing with Type IV hypersensitivity reactions, also known as delayed-type hypersensitivity (DTH). These reactions involve T-cells rather than antibodies and typically develop 24-72 hours after exposure.
Poison ivy contains urushiol, which acts as a hapten - a small molecule that becomes immunogenic only when it binds to skin proteins. During the first exposure, urushiol penetrates the skin and conjugates with cellular proteins, creating new antigens. Antigen-presenting cells process these urushiol-protein complexes and present them to naive T-cells, causing sensitization. This initial process takes 7-14 days and produces no visible reaction. Upon re-exposure, memory T-cells rapidly recognize the urushiol antigens and trigger an inflammatory cascade, leading to the characteristic blistering rash within 48 hours.
Answer A incorrectly suggests an IgE-mediated Type I reaction, but poison ivy reactions aren't immediate and don't involve pre-existing antibodies. Answer C describes Type III hypersensitivity with immune complex formation, but urushiol reactions are T-cell mediated, not antibody-mediated. Answer D treats urushiol as a direct toxin requiring cumulative damage, but urushiol is actually an allergen that triggers immune responses, not a dose-dependent poison.
For pathophysiology exams, remember that delayed skin reactions (24-72 hours) with initial sensitization periods strongly suggest Type IV hypersensitivity. The timeline is your key clue: immediate reactions suggest Type I, delayed reactions suggest Type IV.
- This localized reaction is best classified as which type of hypersensitivity?
Answer: Type III (Arthus reaction)
When analyzing vaccine reactions, you need to consider the timing, appearance, and immune mechanism involved. The key clue here is the combination of timing (6-24 hours), localized inflammation, and the fact this reaction is more severe than previous exposures.
This represents a Type III hypersensitivity reaction, specifically an Arthus reaction (D). This occurs when preformed antibodies (from previous tetanus vaccinations) form immune complexes with the injected antigen at the injection site. These complexes activate complement and recruit neutrophils, causing localized inflammation that peaks around 6-24 hours. The increasing severity with repeated exposures is classic for Arthus reactions, as more antibodies are present from prior immunizations.
Option A (Type II) involves antibody-mediated destruction of cells, like in hemolytic transfusion reactions - not the mechanism here. Option B (Type I) would cause immediate symptoms within minutes due to IgE and mast cell degranulation, plus you'd expect systemic symptoms like hives or anaphylaxis rather than just localized swelling. Option C (Type IV) is T-cell mediated and typically takes 48-72 hours to develop, like in contact dermatitis or tuberculin skin tests - too slow for this timeline.
Remember: timing is crucial for distinguishing hypersensitivity types. Type I is immediate (minutes), Type III peaks at 6-24 hours, and Type IV takes 2-3 days. When you see a localized inflammatory reaction at a vaccination site occurring hours after injection in someone with prior exposure, think Arthus reaction.
- A healthcare worker with no symptoms of active tuberculosis has a positive tuberculin skin test (PPD), showing 15 mm of induration at 48 hours. What can be concluded with the most certainty from this result alone?
Answer: The individual possesses memory T-lymphocytes specific for Mycobacterium tuberculosis antigens.
The PPD test is a classic example of a Type IV delayed-type hypersensitivity reaction. A positive result indicates that the person has been previously exposed to M. tuberculosis antigens and has developed a cell-mediated immune response. This response is mediated by memory T-lymphocytes that recognize the tuberculin antigens upon injection, leading to cytokine release and recruitment of inflammatory cells, causing the characteristic induration. The test does not involve antibodies (B) or IgE (D), and it cannot distinguish between a latent infection and active disease (C).
- Which set of laboratory findings would be most consistent with the suspected diagnosis of serum sickness?
Answer: Decreased serum C3 and C4 levels, elevated erythrocyte sedimentation rate (ESR).
When you encounter a patient developing systemic symptoms 1-2 weeks after receiving foreign protein (like equine antivenom), think serum sickness—a classic Type III hypersensitivity reaction. This immune complex-mediated disease occurs when antibodies form against foreign antigens, creating immune complexes that deposit in tissues and trigger complement activation.
The hallmark laboratory finding in serum sickness is complement consumption. As immune complexes activate the classical complement pathway, C3 and C4 levels drop significantly. The inflammatory response also elevates acute phase reactants like ESR, making option B correct.
Let's examine why the other options don't fit. Option A describes Type I hypersensitivity (immediate allergic reactions). While serum sickness can have urticarial components, the elevated IgE and eosinophilia pattern is more characteristic of anaphylaxis or parasitic infections, not the immune complex disease we're seeing here.
Option C suggests hemolytic anemia with a positive Coombs test and elevated LDH from cell destruction. This doesn't match our patient's presentation of fever, rash, joint pain, and kidney involvement.
Option D mentions normal complement levels, which contradicts the pathophysiology of serum sickness where complement is actively consumed. Anti-histone antibodies are associated with drug-induced lupus, not serum sickness.
Study tip: Remember the "consumption pattern"—whenever immune complexes are depositing and activating complement (serum sickness, lupus nephritis, post-infectious glomerulonephritis), expect to see low C3 and C4 levels. This distinguishes Type III from other hypersensitivity reactions.
- Which statement accurately compares the pathophysiological mechanisms of these two reactions?
Answer: The bee sting reaction is mediated by IgE cross-linking on mast cells, while the poison ivy rash is mediated by sensitized T-lymphocytes.
The bee sting causes a Type I (immediate) hypersensitivity reaction, characterized by IgE-mediated mast cell degranulation. The poison ivy rash is a classic Type IV (delayed-type) hypersensitivity reaction, which is cell-mediated by sensitized T-lymphocytes and macrophages, with a characteristic delay of 24-72 hours. Option B incorrectly assigns Type III and Type II mechanisms. Option C incorrectly attributes the Type IV reaction to histamine. Option D reverses the mechanisms for the two reactions.
- In systemic lupus erythematosus (SLE), tissue damage in organs such as the kidneys is primarily a direct consequence of which pathophysiological event?
Answer: Activation of complement by immune complexes deposited along the glomerular basement membrane.
Lupus nephritis is a classic example of a Type III hypersensitivity reaction. The pathogenesis involves the formation of circulating immune complexes (e.g., anti-DNA antibodies complexed with nuclear antigens) that deposit in various tissues, particularly the glomerular basement membrane of the kidney. These deposited complexes activate the complement system, which leads to neutrophil recruitment and subsequent inflammatory tissue damage. Option B describes a Type II mechanism. Option C describes a Type I mechanism. Option D describes a Type IV mechanism.
- The graph shows the typical time courses for four different types of immunologic skin reactions. A patient develops an indurated, erythematous, and pruritic lesion 48 hours after a patch test for a suspected cosmetic allergy. Which curve best represents the kinetics of this patient's reaction?
Answer: Curve C
The scenario describes allergic contact dermatitis diagnosed via a patch test, which is a classic Type IV delayed-type hypersensitivity reaction. This reaction is characterized by a delayed onset, typically starting after 12-24 hours and peaking at 48-72 hours. Curve C, which begins to rise after 12 hours and peaks at 48-72 hours, perfectly represents this kinetic profile. Curve A represents a Type I (wheal and flare) reaction. Curve B represents a Type III (Arthus) reaction. Curve D represents the late-phase component of a Type I reaction.
- A patient presents with a vesicular, erythematous rash on their wrist, appearing 48 hours after wearing a new nickel-containing watch. A biopsy of the lesion would most likely reveal a perivascular infiltrate predominantly composed of which cell types?
Answer: T-lymphocytes and macrophages
This clinical presentation describes allergic contact dermatitis, a classic example of a Type IV or delayed-type hypersensitivity (DTH) reaction. The hallmark of a DTH reaction is a cell-mediated immune response. Histologically, this is characterized by a perivascular infiltrate of CD4+ T-cells (specifically Th1) and macrophages. Eosinophils and mast cells (B) are features of Type I reactions. Neutrophils recruited by immune complexes (C) are characteristic of Type III reactions. Plasma cells (D) are involved in antibody production but are not the primary effector cells in the lesion of a Type IV reaction.
