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?
2. Mucous membranes & secretions
3. Normal flora
What are 2nd line natural immunity?
1. Innate immune cells
3. Compliment system
4. Antimicrobial substances
What are 3rd Line of defense and considered Acquired immunity?
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
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
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?
What are symptoms of anaphylaxis?
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?
Local immune complex diseases
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
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?
Occurs almost immediately
Type II hypersensitivity response
Occurs within weeks to months
May occur months or years after immunosuppression has been terminated
Type IV hypersensitivity response
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?
-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)
-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?
-Failure of self-tolerance
Breakdown of T-Cell anergy
Release of sequestered antigens