Immunology Chapter: Innate vs Adaptive Immunity

<p>Adaptive immunity is specific and generated after exposure to an antigen. (C)</p> Signup and view all the answers

<p>Dendritic cells act as antigen-presenting cells, bridging innate and adaptive immunity. (D)</p> Signup and view all the answers

<p>Complement activation (A)</p> Signup and view all the answers

<p>NK cells directly kill infected cells, while neutrophils engulf and destroy pathogens. (C)</p> Signup and view all the answers

<p>Epithelial barriers provide a physical barrier to prevent pathogen entry. (C)</p> Signup and view all the answers

<p>Multiple genes contribute to the development of autoimmune diseases. (A)</p> Signup and view all the answers

<p>Organ-specific autoimmune diseases affect a single organ, while non-organ-specific diseases affect multiple organs. (B)</p> Signup and view all the answers

<p>Hormones, particularly estrogens, may play a role in triggering these diseases. (C)</p> Signup and view all the answers

<p>Hormones. (C)</p> Signup and view all the answers

<p>MHC genes play a role in T-cell function and immune responses. (C)</p> Signup and view all the answers

<p>Systemic lupus erythematosus (SLE). (D)</p> Signup and view all the answers

<p>Helper T lymphocyte (A)</p> Signup and view all the answers

<p>Cytotoxic T lymphocytes (C)</p> Signup and view all the answers

<p>They are the primary effector cells in cell-mediated immunity (A)</p> Signup and view all the answers

<p>Limit and prevent immune responses against self-antigens (B)</p> Signup and view all the answers

<p>Humoral immunity (C)</p> Signup and view all the answers

<p>B lymphocyte (A)</p> Signup and view all the answers

<p>Presenting processed antigens to T lymphocytes (B)</p> Signup and view all the answers

<p>Humoral and cellular immunity work together to provide comprehensive immune protection (D)</p> Signup and view all the answers

<p>To act as a B-cell antigen receptor. (A)</p> Signup and view all the answers

<p>To bind to mast cells and basophils, triggering the release of histamine and other inflammatory mediators. (B)</p> Signup and view all the answers

<p>Type III (B)</p> Signup and view all the answers

<p>Drug binding to cell surfaces, forming immunogenic epitopes (D)</p> Signup and view all the answers

<p>IgA (C)</p> Signup and view all the answers

<p>Arthus reaction (D)</p> Signup and view all the answers

<p>They are primarily responsible for the production of antibodies. (D)</p> Signup and view all the answers

<p>2-3 days (A)</p> Signup and view all the answers

<p>IgM is more effective than IgA at activating the complement system. (D)</p> Signup and view all the answers

<p>Both are composed of five basic units held together by a joining chain. (B)</p> Signup and view all the answers

<p>Type IV (D)</p> Signup and view all the answers

<p>Deposition of immune complexes within the glomerulus (D)</p> Signup and view all the answers

<p>The extensive genetic polymorphism within the MHC region. (A)</p> Signup and view all the answers

<p>They can be elicited by both exogenous and endogenous antigens. (C)</p> Signup and view all the answers

<p>B lymphocytes (B)</p> Signup and view all the answers

<p>Type III involves antibodies, while type IV involves T cells. (A)</p> Signup and view all the answers

<p>Direct invasion of pathogens into the affected tissue (A)</p> Signup and view all the answers

<p>Mimicking or blocking the action of the endogenous ligand (A)</p> Signup and view all the answers

<p>Modifying self-antigens, enhancing their immunogenicity (B)</p> Signup and view all the answers

<p>Exposure to parasitic infections may train the immune system to be less reactive to self-antigens (B)</p> Signup and view all the answers

<p>Drugs resemble self-antigens, leading to cross-reactivity of immune responses (C)</p> Signup and view all the answers

<p>Germ-free environments promote the development of autoimmunity (D)</p> Signup and view all the answers

<p>It is likely influenced by genetic factors (D)</p> Signup and view all the answers

<p>They are typically caused by infections (D)</p> Signup and view all the answers

The first line of defense against pathogens, ready to react immediately.

Part of the immune system that adapts after exposure to pathogens for a stronger response.

Cells like neutrophils and macrophages that engulf and destroy microbes.

Receptors that detect specific molecular patterns on pathogens.

A type of pattern recognition receptor that recognizes conserved motifs on pathogens.

Physical barriers (like skin) that block entry of pathogens.

Proteins released by cells that affect the behavior of other cells during immune responses.

White blood cells that are crucial for adaptive immunity, including B and T cells.

Immunity that protects against extracellular microbes and toxins, mediated by B-lymphocytes.

Immunity responsible for defense against intracellular microbes, mediated by T-lymphocytes.

Antigen-presenting cells that initiate T-cell responses by capturing and presenting antigens.

Cells that phagocytose microbes and present antigens to T cells in immune response.

T cells that stimulate B cells to produce antibodies and activate other immune cells.

An immune response where antibodies target self-antigens, often leading to cell destruction.

Types of antibodies that can mediate type II hypersensitivity reactions.

A condition where red blood cells are destroyed faster than the body can replace them, often due to antibodies.

Reactions caused by the formation of immune complexes in tissues, leading to inflammation.

A localized inflammatory response caused by immune complexes after antigen injection in sensitized animals.

An immune reaction mediated by T cells that occurs 2–3 days after exposure to an antigen.

A skin response to PPD in sensitized individuals indicating prior exposure to tuberculosis.

Proteins released by T cells that mediate the inflammatory response in delayed-type hypersensitivity.

IgG binds to antigens and promotes phagocytosis by macrophages and polymorphs.

IgM consists of five basic units, forming a large molecule with 10 binding sites.

IgM mainly neutralizes organisms in blood and activates complement.

IgA protects mucosal surfaces and is found in secretions like breast milk.

IgA is a dimer linked by a 'J chain' and has a secretory component.

IgD acts as a B-cell antigen receptor, mainly found on naive B cells.

IgE binds to mast cells and basophils, playing a role in allergic responses.

MHC molecules determine tissue compatibility and are highly polymorphic.

Autoimmunity triggered by certain drugs that interact with MHC molecules.

Genetic factors that make individuals more likely to develop autoimmunity when exposed to triggers.

Infection may reduce risk of autoimmune diseases in some populations.

Living without germs can promote the development of autoimmunity in models.

UV exposure can trigger skin inflammation and systemic effects in autoimmune conditions like SLE.

Tissue damage in autoimmunity involves antibodies, immune complexes, or T-cell activation.

Antibodies that target self-antigens, potentially disrupting normal function without inflammation.

A type of autoimmunity affecting hormone receptors, leading to function abnormalities.

An immune response against self-antigens causing damage or dysfunction.

Autoimmune diseases that target a single organ or gland.

Diseases affecting multiple organs with widespread autoantigens.

Multiple genes contribute to autoimmune disease, often linked in families.

Major histocompatibility complex alleles are strongly linked to autoimmune diseases.

External factors like hormones that initiate autoimmune responses.

Hormones, particularly estrogens, affect the onset of autoimmune diseases, mainly in females.

An autoimmune disease where hormonal changes can inhibit or accelerate onset.