Immune System

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1
protective defenses
1) physical barriers: skin and mucous membranes
2) mechanical barriers: cilia; body moving bacteria away
3) biomechanical barriers: sweat/tears; saliva/mucous
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innate immunity **
- non specific immunity
- starts at skin
- cells: macrophages, neutrophils, natural killer cells, dendritic cells, intraepithelial lymphocytes
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disorders of phagocytosis
- bacterial and fungal infections
- ex. chronic granulomatous disease: detect microbicidal oxidant production
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** opsonization
- molecular coating: antibodies; allows WBCs to see pathogens better
- enhances phagocytosis
- complement is done through innate immunity
- antibodies are present during adaptive immunity
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complement
- proteins
- ciruclating
- chemotaxis
- opsonization
- amplifying cascade converges on C3 *
- increases vascular permeability
- coagulation
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complement disorders
- encapsulated bacterial infections (strep)
- autoimmunity (lupus)
- hereditary angioedema: excessive fluid outside of cell due to a C1 (protein) deficiency
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adaptive immunity
- antigen specific
- lymphocyte mediated: bone marrow origin -- humoral and cellular immunity
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humoral immunity
- B cell mediated, which is stored in lymph nodes
- antibodies exhibit 'Y' shapred proteins: IgM, IgG, IgA, IgE
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forms of antibodies
- IgM: early, large; usually seen on naive B-cells
- IgG: most abundant, small
- IgA: GI, colostrum
- IgE: activates basophils and mast cells
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humoral immunodeficiency
- B cell dysfunction
- risk of staph, strep, flu
- ex: hypo(low)gammaglobulin(GI)emia(blood) of infancy
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cellular immunodeficiency
- T cell dysfunction
- more severe than humoral immunodeficiency
- risk of virual, fungal, and opportunistic infections
ex: HIV and DiGeorge Syndrome (absent thymus = no T cells)
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combinded immunodeficiency
- B cell and T cell dysfunction usually leads to cancer
- severe combinded immunodeficiency disorder
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passive immunity **
**- transplacental -mother to fetus = IgG
**- IgM is consistent with fetal infection
- breastmilk: IgA and IgG
- monoclonal antibodies from donors (either animal or human)
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aging and immunity
- more susceptible to infection
- decreased vaccine response (ex: have to be give a higher dose of the flu vaccine)
- increased prevalence of autoimmunity
- cancer risk
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Hypersensitivity disorder
allergic reaction; exaggerated immune response
- type 1
- type 2
- type 3
- type 4
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type 1 **
- IgE mediated
- rapid following exposure; classic allergy
- mechanism: TH2 -- B cell differentiation -- IgE production -- mast cellsasophils -- histamine release
- can be local or systemic
- ex. anaphylaxis: life-threatening allergic reaction
- atopy; genetic
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atopy
predisposition to Type 1 reactions
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type 1 triad **
- eczema
- asthma
- allergic rhinitis (hay fever)
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type 1 diagnostics and treatments
Dx: skin prick testing or serology (measuring antibodies in someone's blood)
Tx: desensitization immunotherapy (allergy shots)
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type 2 **
- IgG or IgM mediated
- both gram neg and positive complement, meaning that it can attack cells with both of these cell walls
- ligand replacement (Graves Disease): anitbody attacking self
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type 3 **
- antigen/antibody complex
- too many antibodies being activated
- activates complement cascade
- ex. lupus
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type 4 **
- T-cell mediated
- delayed: can take days or weeks to see symptoms
- ex. contact dermatitis (poison oak)
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transplant immunology
- allograft: from another body
- autograft: from the same body
- rejection: usually type 4
- graft vs host disease: transplanted organ still has T cells from host and attacks patient
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autoimmunity
- immune response to self
- females are more likely than males to have autoimmunity
- hertiable or envi factors (cig smoke exposure, chemicals, formula feeding)
- loss of T-cell anergy: immune system is more likely to attack itself
- molecular mimicry: infection produces immune response to autoantigens
25
autoimmunity dx
- history
- physical
- serology
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HIV/AIDS
human immunodeficiency virus/acquired immunodeficiency syndrome
- virus is enveloped
- contains p24 protein (major protein core encoded in gene)
- attacks T helper cells CD4
- cancer risk; more susceptible to severe infection
- decreased vaccine response
27
HIV/AIDS infection
1) binds to T helper cell
2) internalization of virus
3) uncoating
4) reverse transcription (RNA < DNA)
5) integration
6) transcription
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HIV/AIDS clinical course
- congenital: failure to thrive / developmental delay
- primary infection: fever, sore throat, night sweats
- latency: around 10 years
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HIV/AIDS transmission
- blood to blood
- sexual
- perinatal: mom to baby
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HIV/AIDS seroconversion
people who are high risk should be tested every 1-3 months
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HIV/AIDS prevention
- avoidance
- condoms
- pre-exposure prophylasix (PrEP): medicine taken to prevent HIV
- post-exposure prophlasix (PEP): prevents virus to take hold after exposure
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