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Vocabulary flashcards covering key terms and mechanisms related to Type IV (delayed-type) hypersensitivity reactions.
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Type IV Hypersensitivity (Delayed-Type)
A cell-mediated immune reaction that appears after 12–48 h, driven by sensitized T cells rather than antibodies.
Delayed-Type Hypersensitivity (DTH)
Synonym for Type IV hypersensitivity that emphasizes the slow onset of the response.
Cell-Mediated Immunity
Branch of adaptive immunity in which T lymphocytes, not antibodies, recognize antigen and orchestrate defense.
CD4⁺ TH1 Cell
Helper T cell subset that secretes IFN-γ and other cytokines to activate macrophages in DTH reactions.
CD8⁺ Cytotoxic T Lymphocyte (CTL)
T cell that recognizes antigen with its TCR and kills infected or abnormal cells by releasing perforin and granzymes; may contribute to Type IV reactions.
Interferon-Gamma (IFN-γ)
Key TH1 cytokine that powerfully activates macrophages and promotes inflammation in Type IV hypersensitivity.
Macrophage Activation
Functional shift of macrophages to a highly microbicidal, inflammatory state triggered mainly by IFN-γ in DTH.
Hapten
A small molecule that becomes immunogenic only after binding to host proteins, forming a hapten-carrier complex.
Sensitization Phase
Initial exposure stage (5–10 days) in which antigen is processed by Langerhans’ cells and memory T cells are generated; no clinical signs yet.
Elicitation Phase
Re-exposure stage in which memory T cells rapidly release cytokines, recruit macrophages, and produce visible inflammation within 24–72 h.
Langerhans’ Cell
Dendritic cell in the epidermis that captures cutaneous antigens and initiates the sensitization phase of contact hypersensitivity.
Memory T Cell
Long-lived T lymphocyte generated during the sensitization phase that responds rapidly on re-encounter with antigen in Type IV reactions.
Contact Dermatitis
Eczema-like skin inflammation caused by Type IV reaction to haptens such as nickel, rubber, or poison ivy.
Tuberculin Skin Test (Mantoux Test)
Diagnostic intradermal injection of purified protein derivative (PPD); induration at 48-72 h indicates a TH1 memory response to Mycobacterium tuberculosis.
Granulomatous Hypersensitivity
Late (21–28 days) Type IV reaction in which persistent antigen drives formation of granulomas composed of macrophages, epithelioid cells, and giant cells.
Granuloma
A structured collection of activated macrophages, epithelioid cells, and giant cells formed to wall off indigestible pathogens or material.
Epithelioid Cell
Modified, elongated macrophage with abundant cytoplasm present in granulomas of chronic Type IV reactions.
Multinucleated Giant Cell
Cell formed by fusion of activated macrophages within granulomas; hallmark of chronic Type IV hypersensitivity.
Proinflammatory Cytokines
Mediators such as TNF-α, IL-2, IFN-γ, and GM-CSF produced by TH1 cells during the elicitation phase to amplify inflammation.
Adhesion Molecules (E-Selectin, ICAM-1, VCAM-1)
Endothelial surface proteins up-regulated in DTH that facilitate leukocyte adhesion and migration into tissues.
Induration
Firm swelling at an intradermal site (e.g., positive PPD) produced by cellular infiltrate and edema in Type IV hypersensitivity.
Eczema-Like Rash
Clinical appearance of contact hypersensitivity featuring redness, itching, and possible blistering 24-72 h after exposure.
Patch Test
Diagnostic method where suspected contact allergens are applied to skin under occlusion; reactions read at 48–72 h.
Persistent Antigen
Non-degradable microbe or material that maintains continuous T-cell stimulation, promoting granuloma formation.
TH1 Cytokines (IL-2, GM-CSF)
Cytokines secreted by TH1 cells that promote T-cell proliferation and enhance macrophage function in DTH.
Reaction Time (48–72 h)
Typical interval between antigen challenge and peak clinical response in contact and tuberculin Type IV reactions.
Carrier Protein
Host protein to which a hapten binds, creating a novel antigenic determinant recognized by T cells.
TCR (T-Cell Receptor)
Antigen-recognition molecule on T lymphocytes that binds peptide–MHC complexes during Type IV hypersensitivity.
Complement Independence
Feature of Type IV reactions indicating they are mediated by T cells and macrophages rather than by complement-fixing antibodies.