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Flashcards in Immunity Deck (38):

Differences in T and B cell immunity

B- B cells fright of bacteria and create antibodies

T cells fight off bacteria, Protozoa, fungal infections


What are the first lines of defense in innate immunity?

1. Skin

2. Mucous membranes & secretions

3. Normal flora


What are 2nd line natural immunity?

1. Innate immune cells

2. Inflammation

3. Compliment system

4. Antimicrobial substances


What are 3rd Line of defense and considered Acquired immunity?

Specialized lymphocytes
B cells
T cells (helper T & Killer T)


What are the differences between primary and secondary immunodeficiency states?

Primary (congenital or inherited)—> defect present at birth

Secondary (acquired later in life in response to another diesease or entity/condition)


What are some examples of secondary immunodeficiency?

Neoplasticism disease (lymphoma
Therapies that create high risk for infection (chemo, transplant rejection meds)


In humoral or B cell immunodeficiency, what is decreased and what is a patient at risk for?

Decreased Ig production

At risk for recurrent infections b/c lack of defense against bacterial invasion. (Viral response in unaffected)

B cells fight Bacteria and can be substituted with antiBiotics


How do B cells normal help neutralize infection?

1. Stimulate macrophage for phagocytosis

2. Make specific antibodies


What are the different functions of CD4+ T cells and CD8+ T cells?

CD4+helper T cells —> help immune system work more efficiently

CD8+ cytotoxic T cells —> focused on fugal, viral, intracellular infections —> “trouble fighting off viruses”


Why are Cell mediated T cell immunodeficiencies the most severe?

They impair the ability of the immune system to protect against viral, fungal, protozoan, and intracellular bacterial infections


What is an example of severe combined immunodefiency?

A person who has defects in both humoral and cell-mediated immune responses —> disruption in communication pathways —> severe deficiency

“Boy in the bubble”


What happens as a result of the loss of the compliment system?

Decreased or absent chemotaxis
Impaired opsonization
Decreased phagocytosis of invasive pathogens

*more susceptible to infectious diseases
*leading cause of autoimmune disease


What deficiencies can lead to disorders of phagocytosis?

1. Dec. Leukocyte adhesion

2. Microbial production and activity

3. Cellular degranulation


What is a person more suseptible to if they have disorders of phagocytosis?

-bacterial and fungal infections including candid

-lung disorders


What is immunological mechanism behind allergic response?

Hypersensitivity reaction (4 types)

1. IgE antibodies
2. Modification of cell surfaces
3. Accumulation of antibody-antigen complexes in different tissues
4. Entirely T cell mediated —> takes time


What is the main chemical mediator in type 1 reaction?



What is the difference between anaphylactic and atopic reactions

Anaphylactic- first causes vasodilation, smooth muscle contraction, bronchial dilation, and muscle spasms (5-30 min)—> intense inflammation, epithelial damage, mucosal edema, bronchi spasm (2-8hours)

Atopic- local, causes allergic rhinitis


What is Patho of type one res once?

Antigen/allergen —> IgE antibodies produced —> attach to mast cells and basophils —> release of mediators —> histamine —> inflammatory response —> edema and large amounts of mucus —> constriction of bronchioles


Why is 2nd exposure to allergen worse than 1st?

After sensitization —> IgE abs are already formed and stay in body, more quickly degranulate


What are some changes that occur in the body from type 1 hypersensitivity reactions?

-antibiotic allergies
Food allergies
Hay fever
Urticaria (hives)
Allergic conjunctivitis


What are symptoms of anaphylaxis?

*massive vasodilation*
Headache, sissy ness, parenthesis
Puritis, angioedem, erythema, urticaria
Hoarseness, coughing, narrow airway, wheezing, strider, resp. Arrest
Hypotension, dysrythmias, tachycardia, cardiac arrest
Cramping, n/v, diarrhea


Type 2 antibody mediated disorders/ cytotoxic hypersensitivity are mediated by IgG or IgM, what are different types?

1. Complement-activated cell destruction (phagocytosis or injury)—> Rh incompatibility

2. Antibody-mediated cell cytotoxicity (goodpasture disease)

3. Complement- and antibody-mediated inflammation (Graves’ disease, myasthenia Travis)

4. Antibody-dependent modulation of normal cell surface receptors


What are clinical manifestations of a type 2 hypersensitivity reaction?

If platlets: Heparin induce thrombocytopenia

RBCs: hemolytic anemia, penicillin-induced drug run

Muscle: myasthenia Travis

Thyroid: Graves’ disease


What is Patho behind type 3 immune complex-mediated disorders?

Formation of antigen–antibody complexes in the bloodstream that are deposited in the vascular epithelium or extravascular tissues. —> activate compliment system —> attraction of leukocytes —> massive inflammatory response —> vessel and tissue injury


What are 3 ways that type 3 rxns cause tissue damage?

1. Alterations in blood flow
2. Increased vascular permeability
3. Destructive action of inflammatory cells


What types of injury can occur from type 3 immune response?

Organ damage

Ex: glomerulonephritis
Serum sickness
Local immune complex diseases
Systemic lupus
Reactive arthritis


What are differences in type 4 direct cell-mediated cytotoxicity and delayed type hypersensitivity?

Direct cell-mediated cytotoxicity (CD8+T cells)
Causes cell death and tissue injury in sensitized people
topically administered chemical antigens (contact dermatitis)
systemic antigen exposure
autoimmune process

Delayed-type hypersensitivity
Presensitized CD4+ T cells release cytokines – damaging cells


How long does type 4 hypersensitivity take?

Several days after exposure b/c T cell activation takes time


Type 1 and type 4 both target allergen molecules.. what is the difference?

Type 1 has IGE mediator, immediate
Type 4 is T cells, delayed reaction

Ex: latex allergy can be both type 1, IgE mediated from sensitization to latex protein, or
Type 4- delayed hypersensitivity to rubber additives causing contact dermatitis.


Summary of 4 types

1. Allergic response to allergen molecules with IgE
2. IgM and IgG respond to modified cell surfaces
3. IgG responds to antigen-antibody immune complexes
4. T cells respond to allergen molecules in a delayed reaction


What are the 3 types of transplant rejection?

-Hyperacute Reaction
Occurs almost immediately
Type II hypersensitivity response

-Acute Rejection
Occurs within weeks to months
May occur months or years after immunosuppression has been terminated
Type IV hypersensitivity response

-Chronic Rejection
Occurs month to years later
Manifests with dense intimal fibrosis of blood vessels of the transplanted organ
Type III & IV hypersensitivity reaction


Explain graft vs host disease

Donor T cells on the graft attack recipients tissues

-presents with diarrhea, rash and jaundice


How do automminue disease lead to damage?

Body loses immunologic self tolerance
—> response against host tissues —> affects any cell type, tissue, or organ —> damage


What is the difference between central and peripheral tolerance?

Central tolerance
-The elimination of self-reactive T cells and B cells in the central lymphoid organs (i.e., the thymus for T cells and the bone marrow for B cells)

Peripheral tolerance
-Derives from the deletion or inactivation of autoreactive T cells or B cells that escaped elimination in the central lymphoid organs (thymus)


Explain molecular mimicry as a failure of self tolerance leading to autoimmunity

Molecular mimicry: something happens so body thinks its foreign
-ex: heparin included thrombocytopenia
Body sees heparin complex of foreign —> kills platlets instead


Explain superantigens that lead to failure of self tolerance

Superantigens: tissue antigen
Ex: fat in liver —> body knows it shouldn’t be fatty —> gets attacked b/c body knows it isn’t right
-happens secondary to disease or disorder


What are mechanisms of autoimmune disease?

Susceptibility genes

-Failure of self-tolerance
Breakdown of T-Cell anergy
Release of sequestered antigens
Molecular mimicry


What are 3 criteria for determining an autoimmune disorder?

1. Evidence of an autoimmune reaction

2. Determination that the immunologic findings are not secondary to another condition

3. The lack of other identified causes for the disorder