Mini 3 Immuno High Yield Concepts Flashcards by Neiman Jocindée

T Cell proliferation

IL 2

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Th1 cells

Major role & cytokines

IL 12
IFN-gamma - MACROPHAGE activation
TNF-alpha

Defense against INTRACELLULAR PATHOGENS

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Th2 cells

cytokines & major role

IL 4
IL 5
IL 13

Target cells: eosinophils for allergy
Defense: helminths

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Th17

Cytokines and major role

IL 17
IL 22

Neutrophils!
Extracellular bacteria & Fungi

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Treg

IL10

TGF-beta

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Active Immunity

Natural vs Artificial

Natural: naturally exposed to antigen
Passive: vaccination

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Passive Immunology

Natural vs Artificial

Natural: via mother in utero (IgG, IgA)
Artificial: another animal (pig blood/enzymes)

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Inflammatory cytokines and respective response

IL1: fever/heat
IL6: acute phase proteins
TNF-alpha:

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Describe the 4 steps of the JAK/STAT signaling pathway

1-cytokines receptors are extracellular with cytoplasmic domains that bind JAK
2- cytokines binding DIMERIZES receptor which causes JAK DIMERIZATION which causes JAK autoactivation and autophosphorylation
3-STAT binds to phosphorylated JAK causing STAT to become phosphorylated
4- phosphorylated STAT DIMERIZE and go to nucleus to initiate gene transcription

Key: JAK must be dimerized and phosphorylated
STAT must be dimerized and phosphorylated.
Activated JAK activates STAT

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Cytokines secretes by Dendritic cells

IFN-alpha
IL1
IL10
IL12

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Cytokines for Mo activation

Hint: only thing Mo cannot secrete

IFNy

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Tfh

Cytokines and major role

IL 21
(Secondary INFy & IL4)

B cells for antibody production for EXTRACELLULAR pathogens

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Classical vs Alternative Mo

Classical: IFNy, inflammation, phagocytosis

Alternative: anti inflammatory

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What do Paneth Cells of the GI secrete?

Alpha defensins!!!!
Phospholipase A
Lysozyme

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Genitourinary defense proteins

Tamm-Horsfall protein in urine

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Deficiency in RAG 1 and RAG 2

Omen syndrome

Mutations of the RAG1 and/or RAG2 result in severe combined immune deficiency
complete lack of circulating T and B cells due to an early block in lymphoid development

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NADPH oxidase deficiency leads to

Chronic granulomatous disease: inherited disorder of phagocytosic cells.
Leads to recurrent life threatening bacterial and fungal infections

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Natural Killer Cells

CD16
Use Perforin and granzyme for killing
Inactivated by MHC I on all healthy cells
Virally infected cells inhibit MHC I - engage Fas for killing
Contain FasL

IL-12 role

Activation of NK cells which secrete IFN-y in return

C3 convertase for Alternative Pathway

C3bBb stabilized by properdin (factor p)

Factor B is cleaved by Factor D

Inhibitors of Complement

Pretty much inhibit complement cascades

Factor H opposite effect of properdin….inactivates C3 and C5 convertase (alternative only)

Factor I cleaves C3b and C4b to make inactive….makes iC3b…MCP is cofactor

DAF dissociates C3 convertase by binding to C3b or C4b

CD59 blocks binds to C7&C8 to block C9

C4BP interacts with C4b kicking C2 out

Classical Pathway

Innate immunity via C reactive proteins
Adaptive immunity via antibody binding to Ag

Last to act

Complement components C1 C4 and C2
C3 convertase: C4bC2a
C5 convertase: C4bC2aC3b

Sam convertases as MBL pathway

MBL Pathway

Second to act
MASPS1&2 and man

C3 convertase: C4bC2a
C5 convertase: C4bC2aC3b

Same convertases as Classical

When C5 convertase activated

Membrane Attack Complex

C5bC6C7C8PolyC9

C9 makes the pore!!!!

Lymphocyte-APC receptor Tcell to B cell

APC - CD80/86 —TCell- CD28 Tcell CD40L — Bcell CD40 CD 8 stabilized on CD8 T cells MHC I CD4 stabilizes on CD4 T cells MHC II

Antigen presentation by MHC I and II APC

APC use MHC I for intracellular presentation for CD8...in ER: alpha and beta chain assemble and degraded protein added...surface expression to Th1 MHC II via phagocytosis, CLIP removed from HLA-DM so Ag can replace it...HLA represent Ag on surface to Th2

CD 4 signals | Hint 3

1- Antigen engagement CD 4 + MHC II on APC 2- Costimulation CD 28 on T + CD 80/86 B7 on APC 3- Cytokines JAK/STAT

Treg lymphocytes major role

are responsible for peripheral tolerance, as well as termination of inflammatory responses

Genetics of MHC

Polygenic Polymorphic Co-dominant

Secondary Lymph organs

APC enter via afferent T cells enter via HEV/ artery and housed in parafollicular cortex aka T cell zone B cells enter via artery and housed in lymphoid follicle/germinal center. Germinal center reaction: where they proliferate and become specific Follicular Dendritic Cells present Ag to many B cells at a time

A:b vs yd T cell receptors

Alpha beta recognize peptides and Peptides must be presented in the context of MHC Gamma-delta can recognize peptide or nonpeptide Ag with or without MHC

T cell negative and positive selection

Negative selection is responsible for central tolerance | Negative selection - apoptosis because cannot recognize self or Ag

Secretion and restriction of IL 4

IL 4 from APC | Dendritic cells do not secrete IL 4

Ending T Cell activation

Blocking B7 on APC to CTLA 4 (co stimulatory) | Or instrinsic inhibitory signaling

Immunosenescence

Gradual deterioration of immune system brought by aging

SCID

Deficiencies in T lymphocyte development | Lead to severe combined immunodeficiency (SCID), which are deficiencies in both B and T lymphocytes

DiGeorge syndrome

Deficiency in T lymphocyte maturation

X-linked hyperM

Cannot isotope switch!!!!! | Defects in T cell dependent B cell activation due to mutation in CD40L on T cell

B cell checkpoints

First checkpoint: selects for functional heavy chain/preB chain receptor Second checkpoint: selects for functional light chains Failure = apoptosis Advancement: functional IgM

AID - ACTIVATION INDUCED DEAMINASE (AID)

B cells getting verrrryyyy specific for enzyme The processes of somatic hypermutation and isotype switching are mediated by the enzyme activation-induced cytidine deaminase (AID) The synthesis of this enzyme is controlled by IL-4 and CD-40 activation signals These base changes lead to altered binding affinities. -Those B cells with improved affinity will be clonally selected and will proliferate.

Alpha defensins

Neutrophil peptide proteins for defense

Beta defensins

Antimicrobial for epithelial surfaces

NF-kB and AP1

regulates cellular responses because it belongs to the category of "rapid-acting" primary transcription factors From PLC/DAG Pathway

NEMO

Nuclear factor-kappa B Essential Modulator (NEMO) deficiency syndrome NEMO is the modulator protein in the IKK inhibitor complex that, when activated, phosphorylates the inhibitor of the NF-κB transcription factors allowing for the translocation of transcription factors into the nucleus.