Immunology Flashcards
Isolated Lymphoid Follicles
A single follicle consisting solely of B-cells with an overlying M-cell
*Differs from Peyer’s patches because these are also found in the colon
Effector Cells in the GALT
B-cells from Peyer’s Patch: Travel thru efferent lymphatic to mesenteric lymph nodes, into the blood stream, and back into the GI mucose
T-cells from Mesenteric Lymph Node: Leave and travel to gastric mucosa
Effect B/T-cell Homing
- Effector lymphocytes express a4:B7 which will bind to MADCAM-1 on the endothelial cells of gastric vasculature
- CCL25 secreted by the SI epithelium binds to CCR9 on effector lymphs causing them to move into the lamina propria
- IELs express aE:B7 which binds to E-cadherin expressed by SI epithelium facilitating the movement of IELs
Isotype switching to IgA
TGF-B
Functions of secretory IgA
- Export toxins in the lamina propria
- Neutralize toxins in endosomes
- Bind Ag on mucosal surface
Oral Immunization
=> IgA in GI tract (until colon) AND Mammary glands
Intranasal Vaccination
=> IgA in upper respiratory tract AND cervical-vagina mucosa
Cells of mucosal epithelia
CD8+ T-cells
*Activated effector cells predominate
Gut Tolerance
Refers to the primary fnxn of immune cells in the GALT to restrain and not constantly activate the immune response
CCR7
Molecule lost by naive T-cells when activated by Ag in the MALT; replace it w/ L-selectin
Paneth Cells
Found at the crypts of the small intestinal villi and secrete antimicrobial proteins
Best response to intracellular bacteria
CD4+ Th1-mediated => binds to macrophages inducing heightened ROS species formation, release of inflammatory cytokines, and increased B7 expression
*Innate response includes NK (IFN-y) activation of macs
Best Mechanism for Viral Defense
CD8+ mediated elimination of effected cells thru the release of perforins/granzymes and the binding of Fas-FasL
*Ab response is important before the virus is intracellular and after its release
Best response for Extracellular Pathogens
Mediated by Abs released from CD4+-Th2 cells; release Abs into the bloodstream from the lymph node that fnxn to:
- Activate the classical complement pathway => Anaphylaxis, complement coating
- Bind Ag and macrophages thru the FcR-y
- Opsonization of bacteria
* CD4+-Th1 cells will also release IFN-y and TNF-a
Adaptive Immune Response to Protozoa
Intracellular => Cell-mediated immunity via Th1 activation of macrophages by IFN-y release
Extracellular => Ab release triggering lysis, opsonization, and complement activation
Adaptive Immune Response to Helminths
Mediated by CD4+-Th2 cells AND unique products released by CD4+-Th1 cells including:
- IL-4- promotes isotypic switch to IgE
2 IL-5- activates eosinophils => release of MBP which kills parasites
- IL-13- promotes the alternative activation of macrophages (will now compromise helminth vitality w/ granuloma formation) and increased epithelial mucous production
Best Response to Fungal Infection
Mediated by CD4+-Th1 cells: Activates innate immune responses
- Treg limits response to prevent collateral damage
- Th2 can limit the response leading to fungal persistence
Sialic Acid Residues
Present on the capsules of extracellular bacteria and inhibits complement activation via the alternative pathway
lkB
When bound, inhibits NfkB from activating transcriptional changes; some bacteria can promote IkB binding to inhibit host response
Septic Shock
Caused by the widespread activation of complement and release of IL-1, IL-12, and TNF-a
*Characterized by circulatory collapse and DIC
Antigenic Drift
Gradual mutations that occur to increase the virulence factors of viral antigens
E.g-drift in the hemagglutinin gene
Antigenic Shift
RNA segments are exchanged with a secondary host
=>Rapid change in the form of the protein product produced by a virus
Response to Plasmodium
Sporozites exist in the blood stream => Elimination by complement
Sporozoites infect liver cells => Eliminated by CD8+ T-cells
Merozoites exist in blood => Elimination by antibodies
Response to Leishmania
Exist largely in macrophages and can cause scarring and tissue damage
=>Response mediated by Th1
Overreaction to Parasites
- Can result in nephrotic syndrome due to deposition of immune complexes
- Cross-recognition of peripheral nerve tissue
- Hepatosplenomegaly
Long IgA1
Flexible, but susceptible to cleavage
Opposite for IgA2
Dendritic Cells in the absence of extracellular bacterial infxn
Secrete TGF-B which causes FoxP3 to be expressed in CD4+ cells turning them into Treg cells
Dendritic cells in early bacterial infection
Produce IL-6 which causes CD4+ cells to express RORyt causing CD4+ cells to become Th17 cells
PPARy
Protein that removes NFkB from the nucleus; can be activated by bacteria as a defense mechanism
Activators of PMNs
LTB4
C5a
IL-8
Bacterial peptides
