Module 11: Hypersensitivities and Immunodeficiencies Flashcards

This set of vocabulary flashcards covers types of hypersensitivities, primary and secondary immunodeficiencies, specific autoimmune disorders like SLE and HIV/AIDS, and transplant-related immune responses.

Type I Hypersensitivity

An immediate allergic reaction mediated by IgE antibodies that bind to mast cells and basophils, causing the release of histamine and other inflammatory mediators upon subsequent exposure.

Anaphylaxis

A severe Type I hypersensitivity manifestation characterized by bronchoconstriction, severe vasodilation, hypotension, and potential airway obstruction.

Type II Hypersensitivity

An antibody-mediated reaction where IgG or IgM antibodies attack the body's own cells or tissues, causing cell destruction through complement activation or phagocytosis.

Type III Hypersensitivity

An immune complex-mediated reaction where large numbers of antigen-antibody complexes circulate and deposit in tissues, activating complement and causing inflammation and vasculitis.

Type IV Hypersensitivity

A delayed T-cell mediated reaction that typically develops $24$ to $72$ hours after exposure, involving helper T-cells, cytokines, and cytotoxic T-cells.

Primary Immunodeficiency

Inherited genetic disorders present at birth where one or more components of the immune system are absent, defective, or suppressed.

Secondary Immunodeficiency

An immune impairment that develops later in life due to external factors such as HIV/AIDS, malnutrition, burns, cancer, or chemotherapy.

Selective IgA Deficiency

A primary immunodeficiency characterized by decreased production of IgA antibodies, resulting in recurrent respiratory, sinus, and ear infections.

DiGeorge Syndrome

A primary immunodeficiency caused by the failure of thymus development, leading to deficient T-cell production and increased susceptibility to viral and fungal infections.

Severe Combined Immunodeficiency (SCID)

A primary immunodeficiency characterized by a deficiency of both T-cell and B-cell immunity, often requiring bone marrow or stem cell transplantation.

Systemic Lupus Erythematosus (SLE)

A chronic autoimmune disease classified as a Type III hypersensitivity where autoantibodies form against self-antigens, particularly nuclear components of cells.

Serum Sickness

A Type III hypersensitivity reaction resulting from the formation of antigen-antibody complexes in the bloodstream following administration of foreign proteins or antiserum.

HIV (Human Immunodeficiency Virus)

A retrovirus that primarily attacks CD4 helper T-cells, leading to a secondary cell-mediated immunodeficiency.

Reverse Transcriptase

An HIV enzyme that converts viral RNA into host-compatible DNA during viral replication.

Integrase

An HIV enzyme responsible for inserting viral DNA into the host cell's DNA.

Protease

An HIV enzyme that packages viral RNA into new virions before they bud from the host cell.

HAART (Highly Active Antiretroviral Therapy)

A combination treatment involving multiple drug classes, such as integrase and protease inhibitors, to suppress HIV replication and preserve CD4 counts.

Human Leukocyte Antigens (HLA)

Proteins found on cell surfaces as part of the Major Histocompatibility Complex (MHC) that help the immune system distinguish self from non-self.

Hyperacute Rejection

A humoral transplant rejection that occurs immediately after reperfusion, mediated by pre-existing antibodies similar to a Type III hypersensitivity.

Graft Versus Host Disease (GVHD)

A condition where donor T-cells recognize and attack the recipient's HLA antigens, often occurring after bone marrow or stem cell transplantation.

Autoimmunity

The failure of the immune system to distinguish self from non-self, resulting in immune attacks against the body's own tissues and organs.

Molecular Mimicry

A factor in autoimmunity where microbial antigens resemble self-antigens, causing the immune system to attack both the microbe and the body's tissues.

Superantigens

Exotoxins produced by Staphylococcus and Streptococcus that can cause excessive activation of T-cells and promote autoimmune responses.

Plasmapheresis

A treatment method that removes circulating autoantibodies from the bloodstream to manage autoimmune conditions.