Chapter 6 pt 1 Flashcards
location of dendritic cells
in epithelia, lymphoid organs and most tissue
role of NK cells
early protection against many viruses and intracellular bacteria
innate lympohid cells
look like lymphocytes but have features of innate immunity
plasma proteins
complement
mannose binding lectin
CRP
lung surfactant
complement system innate and adaptive
innate by alternative and lectin path
adapative uses classical pathway by recognizing microbes coated with Abs
TLRs signal via NF-Kb and what else
Interferon regulatory factors which stimulates the production of antiviral cytokines (type 1 interferons)
NLR signal via what and can play a role in what
inflammasome pathway
gout
obesity associated type 2 diabetes
atheroscelrosis
inflammasome pathway
1) NLRP3 recognizes pathogenic bacteria or extracell ATP
2) recruit adapter protein (X2) and inactivated caspase-1 (X2)
3) caspase-1 becomes activated and cleaves Pro-IL1B to IL-1B
4) IL-1B secreted and causes accute inflammation and fever
where is C-type lectin receptors located and on which cells
what does it detect
on PM of macrophages and dendritic cells
detects fungal glycans and elicit inflammatory reactions
G protein coupled receptors that recog microbes are on what cells
and recognize what microbes
neutrophils macrophages and most leukocytes
recognize bacterial peptides containing N-FMEt
B lymphocyte functions
neutralization of microbe with Abs
phagocytosis
complement activation
helper T cell function
activation of macrophages
inflammation
prolif and diff of T and B cells
what is clonal selection
when a lymphyocyte is exposed and responds to one antigen it undergoes this and proliferates
-all the “clones” recognize the same antigen
lymphocyte diversity: enzymes that are recomb
RAG-1 and RAG-2
majority of lymphocytes in blood and tissue are
T lymphocytes
TCR 2 types
95% are made up of a and B polypeptide chain
small population are yd
what do yd TCR receptors recognize
- where do they aggregate
- assistance or no assistance MHC proteins
Lipids, peptides, and small molecules
without assistance from MHC proteins
aggregatie at epithelial surfaces
NK T cells recognize what dsiplayed by what
glycolipids displayed by MHC like molecule CD1
which is more prevelenat CD4 or CD8
CD4: 60%
CD8: 30%
innate lymphoid cells produce what cytokines
IFN-y
IL-5
IL-17
IL-22
functions of innate lymphoid cells
early defense against infections
recognize and eliminate stressed cells
provide cytokines that influence differntiation of T lympocytes
what are innate lymphoid cells
populations of lymphocytes that lack TCRs but produce cytokines similar to T cells
NK cells are first defined
what happens in the bone marrow
production of all blood cells and where B lymphocytes mature
what is the main fnct of peripheral lymphoid organs
concentrate antigens, APCs, and lymphocytes in same spot
-optimizes interactions amoung these cells
dendritic cells and LN
dendritic cells pick up and transport antigens of microbes from epithelia and tissue via lymphatic vessels to lymph nodes. migrate to T cell zones and present them to T cells
in the spleen antigens are trapped by ____ and ___
macrophages and dendritic cells
recognize bloodborne antigens
where are 1/2 of the body’s lymphocytes
what types of cells are many of these
in the mucosal tissues, many are memory cells
what do B cell receptors recognize
proteins, polysaccharides and lipids
process of antigen presentation and prolif of T cells
APC presents to naive T cell with costimulation and cytokines
naive T cell expresses high affinity IL-2R and secretes IL-2 (autocrine)
causes prolfieration into effector and memory cells
which T helper subset is involved in IBD, psoriasis and granulomatous inflammation
Th1
which t helper subset is involved in IBD, psoriasis, and MS
Th17
type 1 hypersensitivity Abs produced and others released
IgE
vasoactive amines
mediateors from mast cells
type II HS Abs released
IgG and IgM bind to antigen on target cell
-phagocytosis or lysis of target
type II prototypical disorders
autoimmune hemolytic anemia
goodpasture syndrome
unmatched blood transfucsion
type III HS disorders
SLE, some glomerulonephritis, serum sickness, arthus reactions
type IV HS disorders
contact dermatitis, MS, T1DM, tuberculosis`
type 1 HS reactions (2)
immediate: vasodilation, vascular leakage, SM spasm, glandular secretion
- minutes after exposure, subsides in few hours
late-phase reaction
without additinal exposure to antigen
last several days
infiltrate tissue with BEN monocytes and cd4+ T cells
besides IgE what else are mast cells triggered by
complement components (C5a and C3a) chemokines (IL-8) drugs (codeine and morphin) adenosine melittin (in bee venom) physical stimuli (hot, cold, sunlight)
8 DAMP coochie
Th2 cells nad IL-4
stimulates class switching of B cells to IgE promotes development of additional Th2 cells
IL-13 from Th2 cells
enhances IgE production
acts on epithelial cells to stimulate mucus secretion
crosslinking of FceR1 receptor on mast cell downstream signaling
cytokine gene activation–>cytokines and chemokines secreted (late phase reaction)
signals activation of phospholipase A2 which leads to production of Arachidonic acid and PAF
-arachdonic acid forms PGD2 and LT B4,C4,D,4 (late phase reaction)
signals for degranulation
-histamine, proteases (immediate reaction)
what are in the preformed mast cell granules
histamine: intense SM contraction, increased vascular perm, increased mucus secretion
enzymes neutral proteases (chymase and tryptase) and acid hydrolases
- tissue damage
- act on precursor proteins to make
- kinins and C3a
proteoglycans
-heparin
chondroitin sulfate
lipid mast cell mediators LT and prostaglandins and ___
LT C4 and D4: most potent vasoactive and spasmogenic agents known
prostaglandin D2
-intense bronchospasm and increased mucus secretion
PAF: platelet aggregation, release of histamine, bronchospasm, incresaed vascular permeability, and vasodilation
PB HIV
mast cell cytokines produced
TNF, IL-1 and chemokines
- leukocyte recruitment (late phase rxn)
- inflammatory cells release additional waves of mediators and cause epithelial cell damage
IL-4
-amplifies Th2 response
late phase reaction ____ recruited without what
leukocytes recruited without antigen
what cells in late phase reaction damage tisue and via what
eosinophils via proteases, MBP, and eosinophil cationic protein
how do you treat late phase reaction
with anti-inflammatory drugs
anti-histamine only good for immediate rxn
people with increased atopy have higher what and more what
IgE levels and more Il-4 producing Th2
non-atopic allergy
triggered by what
what cells
20-30% of immediate hypersensitivity rxns
triggered by non-antigenic stimuli like temperature extremes and exercise
no Th2 or IgE
thought due to mast cells that are abnormally sensitive to activation
examples of disorders caused by immediate hypersensitivity
anaphylaxis bronchial asthma allergic rhinitis, sinusitis hay fever food allergies
type II HS Abs (2 types)
autoantibodies or antigbodies to exogenous antigens such as chemical or microbial proteins
mechanisms of Ab mediated injury
1) opsoniztion of cells by Abs and complement components and ingestion by phagocytes
2) inflammation induced by Ab binding to Fc receptors of leukocytes and by complement breakdown products
3) antireceptor antibbodies disturb normal fnct of receptors
(graves disease and myasthenia gravis)
Ab mediated cell destruction and phagocytosis in disease (type II HS)
Transfusion reactions
-cells from incompatile donor react with and opsonized by preformed abs in host
hemolytic disease of newborn (erythroblastosis fetalis)
-maternal IgG anti erythrocyte Abs cross placenta and cause destruction of fetal red cells
certain drug reactions
-drug acts as hapten by attaching to PM of red cells and Abs produced against the complex
Ab mediated inflammation in disease (Type II HS)
glomerulonephritis, vascular rejection in organ grafts
antigens for type III HS
can be endogenous or exogenous
immune complex mediated diseases preferentially involve
kidney (glomerulonephritis)
joints (arthritis)
small blood vessels (vasculitis)
immune complex disease pathogenesis
complement fixing antibodies (IgG and IgM)
-induce pathologic lesions of immune complex disorders
complement proteins and immune complex disease
copmlement proteins detected at site of injury
consumption in active disease–> decreased serum levels of C3
-monitor disease activity
T cell mediated hypersens damage
inflammation from cytokines produced by CD4+ T cells and cell killing by CD8+ T cells
what are the diseases in type 4
one more round of IPC
diabetes type 1, MS, rheumatoid arthritis, IBD, psoriasis, contact dermatits
IFN-y activated macrophages do what
enhance ability to phagocytose and kill microbes
express more MHC class II
secrete TNF, IL-1 and chemokines–>inflammation
produce more IL-12–>amplified Th1 response
what cytokine from Th17 is produced to amplify Th17 response
IL-21
classic example of DTH is what
tuberculin reaction
tuberculous infection has what cells dominate after 2-3 weeks
macrophages, fuse to make epitheloid cells, and these surrounded by lymphocytes called granuloma
granulomatous inflammation is associated with strong ____ cell activation and high level of cytokines like
Th1 cell
IFN-y
CD8+ t cell mediated diseases
type 1 diabetes and graft rejection after organ transplantation
Cd8+ cells plays role in what
reactions against virus (can cause cell damage) and killing of tumor cells
gut microbiome due what
play important role in local and systemic immune functions brain development (gut-brain axis) metabolic functions hormones and neurochem production biofilm
gut microbiome formed by
influence by mode of delivery
child diet
by 3-4 it is adult like
maintained and altered by dietary changes
dysbiosis
alteration of body’s microbial community that decreases pop of good bacteria, and allows bad bacteria to flourish
