52-Granulocytes and Protein Components Flashcards by Adam Rasmussen

Overactive granulocyte activation

Allergic symptoms

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Overactive pathogen sensing receptors

Autoimmune disorders

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Defects in protein components

Increased risk of infection

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granulocytes

eosinophils, basophils, mast cells

Contains large granules that are released non specifically upon activation

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What do granulocytes protect

Epithelial and mucosal surfaces from multicellular parasites and mucosal pathogens

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Role of mast cells

Sentinels

Recruit eosinophils and basophils

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Activation of mast cells

Production of IgE antibodies from antibody producing B cells after encountering pathogen
IgE antibodies bind Fc epsilon receptor to release histamine

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Activation of eosinophiles

Priming with cytokines, soluble Its, or pattern recognition receptor ligans
Activation with immobilized Its, microbial produces, interim engagement, cytokine mediators

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Function of inflammatory mediators

Create hostile environment for pathogens that are too big to eat
Directly kill pathogen
Further activate immune response

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Function of histamine

Alter smooth muscle contraction, vascular permeability, and neuron function

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Inflammatory mediators

Histamine
Protease and antimicrobial peptides-kill pathogens
Lipid mediators
Cytokines-alter function of immune cells
chemokines-recruit other cells

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Inappropriate granulocyte function

Linked to human disease

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What causes allergies and asthma

eosinophils and mast cells

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Drugs that inhibit granulocyte function

Antihistamines
anticytokine drugs
NSAIDS
croticosteroids

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Type 1 interferon release

Antiviral response
Detected by toll like and RIG-I receptors
Induction of genes encoding type 1 IFNs
Release of IFN into environment and binding to receptor

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What happens after IFN bind receptor

Activation of downstream signaling pathways JAK/STAT

Induction of IFN stimulated genes (ISGs)

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What drives the transcription of type 1 INF

IRF3, IRF7, NF-kB, and MAP kinase pathways

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Function of IFN

Upregulated ISG
Stimulate antigen presenting cells
Enhance functions of NK, T, and B cells

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What does up regulation of ISG do

Suppress viral function by blocking replication cycle

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What does stimulation of antigen presenting cells do

produce inflammatory cytokines and enhance presenting function

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What do NK, T and B cells do

NK and T-target and kill

B-produce antibodies

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defensins

Small antimicrobial agents
Positively charged
Bind to negative pathogen membrane
Form pore to destroy pathogen

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cathelicidins

Small antimicrobial agents
Positively charged
Bind to negative pathogen membrane
Form pore to destroy pathogen

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Where are defensins and cathelicidins found

Neutrophils, macrophages, mast cells
paneth cells
keratinocytes

Defensins and cathelicidin in neut, mac, and mast

In primary and secondary granules

Defensins and cathelicidins in paneth cells

In crypts of small intestine Large quantities of defensisns Suppress growth of commensals and pathogenic in mucosal tissue

defensisns and cathelicidns in keratinocytes

Decrease the growth of pathogens on the surface of the skin

Collectins

antimicrobial form trimer with ficolin and then higher order complex increase phagocytosis or complement binding

ficolins

antimicrobial form trimer with collectins and then higher order complex increase phagocytosis or complement binding

antimicrobial proteins

ficolins Surfactants Mannose binding lectins collectins

function of collectins and ficolins

form trimers and higher order complex to increase phagocytosis and complement binding

avidity effect

increase affinity of entire complex by forming higher order structures

what do ficolins bind to

N acetyl glucosamine

what do mannose bind to

mannose derivatives

what do surfactants A and D bind to

mannose and glucose derivatives

what do human glycoproteins contain

galatose, fructose, and sialic acid

how do collectins and ficolins find pathogens

different sugars on surface than humans n acetyl glucosamine, mannose, glucose vs. galatose, fructose, sialic acid

complement system

30 proteins produced by liver protein pathway in the innate response kill pathogens and enhance immune function

what increases expression of complement protiens

infection and inflammation

3 methods of complement activation

lectin, classical, alternative

4 outcomes of complement activation

inflammation and chemoattraction phagocytosis membrane attack complex antibody production

common complement cascade starting at C3

C3 cleavage into C3a and C3b C3b stays on pathogen and coats it to enhance phagocytosis (opsinization) C3b recruits C5 and cleaves into C5a and C5b C5b recruits C6, 7, 8, 9 C9 forms a pore C3a and C5a function as inflammatory mediators and chmoattractans

membrane attack complex

formed from polymerization of C9, bursting pathogen cells effective against gram negative and enveloped virus gram positive is immune

activators of classical pathway

antibodies IgM, IgG1, IgG3, or pentraxin | IgA and IgE do not activate

steps in classical pathway

binding of antibody/pentraxin recruit C1 complex (C1q, C1s, C1r) recruitment of C1 complex cleaves C4 into a and b C4b binds and cleaves C2 C4b/C2b complex serves as C3 convertase complex

pentraxins

proteins found in blood that resemble antibodies | C reactive protein

C1q

classical pathway | binds antibodies or pentraxin

steps in lectin pathway

activated by collectins or ficolins which are bound to MASP 2 and 3 which cleave C4 C4b stays and binds C2 which gets cleaved C4b/C2b form C3 convertase complex

activators of lectin pathway

collectins or ficolins to sugar residues

steps in spontaneous activation pathway

C3 spontaneously cleaved by water, C3b binds to nearest surface C3b binds complement factor B which cleaves into Bb and Ba C3b/Bb form C3 convertase complex

goals of spontaneous activation pathway

amplify classical and lectin pathways | antibody independent pathway

regulators of classical and lectin complement pathway

C1 INH, C4bp inhibit C1 complex and C4b

regulators of spontaneous complement pathway

Cr1, DAF, MCP on surface of cells and factor H and I in blood

lack of complement proteins

increased bacterial infections

deficiencies of proteins in classical pathwya

autoimmune disorders

polymorphisms in suppressive factors

age related macular degeneration | atypical hemolytic uremic syndrom

deficiency in what factors cause increased susceptibility to infections

B, D, 3, 5, 6, 7, 8, 9 | especially Neisseria

deficiency in what factors cause disease that resembles lupus

1, 2, 4