sys5 notes-1

secondary because of memory. They learn antigen characterisitics

recognizze a large number of antiens via gene rearrangement.

• alpha beta
• gamma delta for musocal-5%

hevay and light chains

Ags must be presented to T-cells and B-cells in context of MHC complex

negative selection gone worong in thymus

• 1. lymphoid progenitor
• 2. commonmyeloid progenitor
• 3. common myelodi>myeloblast>monocyte>macrophage
• 4. common myeloid progenitor>megakaryocyte>thromobocytes

mostly memory t-cells. If bone marrow infected in trouble

calor, dolor, rubor, tumor, increased permeability, adhesion, extravsation fo PMNs, macrophages

dentritic cells, macrophages, B-cells( can be activated in t-cell dependent or independent manner)

• MHC antigen presentation.
• Co-stimulatory molecules B7-CD28
• cytokiens

allow t-cells to be fully  activated and survive longer

95% negatively selected for

• None when first in thymus
• they bithe CD4/CD8
• then only one

when t-cells or b-cells are fully activation. central pricniple of adaptive immunity

B-cells get Ag binding and T-cell activation

neutralization, opsinization, activation of complment

MHC class I for virus or can see and directly kill bacteria

cause lysis

• Th1- INF-y and IL-2 inflammation macrophage
• Th2- LI4,6,10 for B-cell activation
• Th17- IL-17 acitvation of PMNs ORAL cavotu
• T reg- inhibit overactivation of T-cells

T-regs

extracellular vs intracellular

• thymus
• bone marrow

• lymph nodes
• spleen
• mucosal and cutaneous lymhoid tissues

macrophage and DCs

• skin and mucosa
• musocal sites have specific antibodies(IgA) and mucin that prevents bacteria from sticking

DCs encounter PAM(some repetitive motif). Signaling cause DCs to move to lymph nodes

t-cells enter via HEVs

t-regs

promote intracellular killing of bacteria in macriohages

drive B-cells to differentiate and drives B-cells to produce antibodies

• need helper t-cells
• first have IgM then class switch

specific for an Ag so its produces more of a receptor

function dependent, particular pathogens and cytokines drive the diff isoforms

memory and then immune sys goes to basal state

herpes, can persist by ceasing to replication until immunty wanes, resist descruction.

inappropriate immune response can lead to persisient disease

virus escapes phagosome.

• leprosy( tuberculoid vs lepromatous leprosy)
• tuberculoid Th1 response,
• lepromatous generates Th2 response

• hypersensitive
• decfective immune system
• gene defects
• autoimmunity

• reaction against NONinfectious antigen.
• IgG or IgE
• susceptibility genes

Th2 type primming

primary due to mutations in genes that are important in controlling response.

due to failure of intrinsic tolerance mechanism

effector t-cells start recognizing and start killing beta cells

IgG, IgE, or specific t-cells

allergies, and anaphylactic type mediated by IgE mass cells and basophils

antibody dependent, directed against antibody to fixed tissue

like type II but response against soluble antigen

T-cell mediated, sensitived T-cells, graft rejection, asthma, contact dermatitis

• mast cell activation to produce IgE:
• allergen crosslinks

release of vasoactive amines (histamine) from basophils and mast cells

the involve recruitment of inflammatory cells and damage

• IgE binds to mast cell to Fc. Acivates mast cells.
• Amount and location of allergen

• reside near mucosal surfaces.
• binding of Ag-Ab-FcR on mast cell triggers a granule to relelase its contents

• increased vascular permeability
• vasodilation
• mucus production
• bronchorestriction

proteases-tryptase kinins and complement components

chemtactic ffactors for recruitment of neutrophil and eosininophil

• prostaglandin, leukotrienes, histamine, etc.
• cytokines (mast cells secrete TNF-a, IL-1, Il-4,6,5,)

• some of these signals lead to b-cell switching
• and activate PhosA2 to AAcid

augments secondary response

• augments inflame response
• vasocontriction
• broncocontriction

• intracellular pathogens (T-cells)
• CD8
• CD4Th1- macrophages
• CD4Th2-class switching

• extracellular microbes and toxins,
• B-cell

bone marrow and thymus

migrating DCs and marophages to lymphnodes

epithelia activate pathways to inflammation and recruitment

with repeated exposures, a host will produce antibodies of greater affinity(somatic hypermuation and clonal selection)

neutralization or opsinization

Type IV hypersensitivity reaction

HLA and MHC

IgG or specific T-cells

• anaphylactic, allergy IgE, Th2 activate class switching
• IgE-Ag-mast cell binding

Ab dependent to fixed tissue

immune complex

cell-mediated, delayed

• 5-30 minutes, basophils and mast cells
• late recruitment of inflamm cells and epithelial damamge

• degranulation>histamne
• late phse>cytokines> TNF-alpha, IL-1,4,5,6, leukotrienes and prostaglandins

leukotriene and prostaglandin

type I,


complement cause cause granule release

initital binding to basement membrane, membrane thickeding, edema, increase in gland sixe and hypertrophy of branchial muscle walls

systemic vasodilation

flare-wheal-flare

IgG An direct cell surface binding

• Graves (AB mediated stimulation
• drug

• AB against basment membrane in kidney and lung (teens-20s, male)
• glomernephrisits and intersitital pnemonia

• complment dependent rxns
• AB mediated cellular dysfunction
• -direct cell lysis or opsination and phago

Ab against desmosomal proteins lead to complement. Blisters  and lesions in oral and genital mucosa IgG

blisters form do not rupture, elderly, IgG hemidesmosomes

• myasthenia gravis block Ach receptor sites
• Graves

• opsinization
• complement/inflamm
• cell dysfunction

• cells from incompatible donor are opsinized (hemolytic disease of newborn diff igGs b/t mother and fetus)
• thrombocytopenia...Abs to own RBCs

• Goodpastures
• Pemphigus vulgaris

myastenia gravis, Graves

III against a soluble antigen via Immune complex

• leading to complement activation and PMN actvity 
• symptoms: fever, rash, arthritis, glomernephritis

small vessels, joints, kidnet, heart

PMN infiltrate, nectrotizing tissue, vasculitis

• serum sickness, strep glomerlonephritis, 
• chronic exposure- lupus
• local complex- arthus only skin necrosis

fever vasculitis, arthitis, nephritis

type III