Alterations in Immunity and Inflammation

Comprehensive vocabulary flashcards covering alterations in immunity and inflammation, including hypersensitivity mechanisms, autoimmune disorders, alloimmunity, and immunodeficiencies.

Allergy

An exaggerated immunologic response against an environmental antigen.

Autoimmunity

A misdirected immunologic response against the host's own cells.

Alloimmunity

An immune response directed against beneficial foreign tissues, such as blood transfusions or organ transplants.

Immunologic Homeostasis

The steady-state of tolerance to self-antigens or the lack of immune reaction against environmental antigens.

Sensitization

The state in which an adequate amount of antibodies or T cells is available to cause a noticeable reaction upon reexposure to an antigen.

Immediate Hypersensitivity Reaction

A reaction that occurs within minutes to a few hours after exposure to an antigen.

Delayed Hypersensitivity Reaction

A reaction that takes several hours to appear and reaches maximum severity days after exposure to an antigen.

Anaphylaxis

A severe, rapid systemic or cutaneous immediate hypersensitivity reaction developing within minutes after exposure to a sensitized antigen.

EpiPen (Epinephrine Auto-Injector)

An emergency medical device containing epinephrine used for immediate treatment of anaphylaxis.

Type I Hypersensitivity

An immunoglobulin E (IgE)-mediated allergic reaction where IgE binds to Fc receptors on mast cells, triggering degranulation and release of primary and secondary mediators.

H1 Receptors

Histamine receptors that mediate bronchial constriction, edema, and vasodilation during Type I hypersensitivity reactions.

H2 Receptors

Histamine receptors that increase gastric secretions and decrease the release of histamine from mast cells and basophils.

Type II Hypersensitivity

A tissue-specific hypersensitivity reaction where antibodies bind to specific target antigens on cell surfaces or tissues, causing cell destruction or altered cellular function.

Neutrophil-Mediated Damage

A Type II hypersensitivity mechanism where antibody-complement binding in tissues leads to neutrophil chemotaxis, adherence, and release of lysosomal enzymes and reactive oxygen species.

Antibody-Dependent Cellular Cytotoxicity (ADCC)

A Type II hypersensitivity mechanism where non-specific cytotoxic cells (such as NK cells) recognize bound IgG antibodies on target cells via Fc receptors and trigger apoptosis using perforin and granzymes.

Type III Hypersensitivity

An immune complex-mediated reaction where circulating antigen-antibody complexes are deposited in vessel walls or extravascular tissues, activating complement and recruiting neutrophils.

Intermediate Immune Complexes

Moderate-sized antigen-antibody complexes that are not easily cleared by macrophages or kidneys, causing tissue deposition and inflammation in Type III hypersensitivity.

Serum Sickness

A systemic Type III hypersensitivity disease caused by circulating immune complexes that affect blood vessels, joints, and kidneys.

Arthus Reaction

A localized Type III hypersensitivity reaction caused by locally injected antigen reacting with IgG, leading to complement activation, neutrophil accumulation, edema, hemorrhage, and tissue damage.

Type IV Hypersensitivity

A cell-mediated delayed reaction where T lymphocytes (Tc cells or Th1/Th17 cells) directly kill target cells or recruit macrophages via cytokines.

Atopic

A genetic predisposition to develop hypersensitivity or allergic reactions against environmental antigens.

Systemic Lupus Erythematosus (SLE)

A chronic multisystem inflammatory autoimmune disease marked by autoantibodies against host DNA and cellular components, classically presenting with a facial malar rash.

Antinuclear Antibodies (ANAs)

Autoantibodies directed against nuclear components of host cells, commonly present in systemic lupus erythematosus (SLE).

ABO Incompatibility

An alloimmune transfusion reaction occurring when isohemagglutinins (IgM antibodies) attack mismatched A or B carbohydrate antigens on donor erythrocytes.

Universal Donor

Blood Type O, which lacks both A and B antigens on erythrocytes and can be transfused to any recipient.

Universal Recipient

Blood Type AB, which possesses both A and B antigens and lacks anti-A and anti-B antibodies in plasma.

Hemolytic Disease of the Newborn

An alloimmune condition resulting from an Rh-negative mother producing anti-D antibodies against an Rh-positive infant's erythrocytes.

Warm Autoimmune Hemolytic Anemia

An autoimmune condition in which IgG antibodies react with erythrocytes at normal body temperature.

Cold Autoimmune Hemolytic Anemia

An autoimmune condition in which IgM autoantibodies react with erythrocytes in cooler portions of the body.

HLA-DR Locus

The human leukocyte antigen locus whose matching is most critical for tissue graft acceptance.

Hyperacute Rejection

An immediate and rare transplant rejection caused by preexisting recipient antibodies against graft antigens.

Acute Rejection

A cell-mediated graft rejection response directed against unmatched donor HLA antigens.

Chronic Rejection

A graft rejection occurring over months or years due to a weak cell-mediated reaction against minor HLA antigens.

Primary Immunodeficiency

A congenital immune defect usually resulting from a single gene mutation, characterized by recurrent, severe infections.

Severe Combined Immunodeficiency (SCID)

The most severe primary immunodeficiency, characterized by a total lack of T-cell function along with partial or total lack of B-cell function.

DiGeorge Syndrome

A primary combined deficiency with nonimmunologic abnormalities marked by a partial or complete absence of T-cell immunity due to thymus hypoplasia or aplasia.

Bruton Agammaglobulinemia

The most severe form of predominantly antibody deficiency, leading to severe loss of immunoglobulin production.

Chronic Mucocutaneous Candidiasis

A primary defect of T lymphocytes characterized by an inability to respond to the yeast Candida albicans.

C3 Deficiency

The most severe complement deficiency because C3 unites all pathways of complement activation and provides C3b, a major opsonin.

Secondary Immunodeficiencies

Acquired immune deficiencies caused by non-genetic external conditions, such as stress, malnutrition, malignancies, infections, or medical treatments.

Graft vs. Host Disease (GVHD)

A fatal condition in immunocompromised recipients where mature T cells in donor graft tissue mount a cell-mediated attack against recipient tissues.