Lecture 41+42+DLA Flashcards
naïve T cells
stimulated by the microbial antigen in lymph nodes and spleen
express L-selectin
express CCR7 a chemokine receptor
effector T cell
migrate to the site of infection
express E and P selectin
integrin LFA-1 and VLA-4
chemokine receptor changes
IFN gamma
stimulate phagocyte mediated ingestion
expression of lysosomal proteases
synthesis of ROS
Ab production for phagocytosis
Stimulate expression of Class II MHC and B7 on APCs (amplify T cell response)
activated macrophages produce IL-12
intracellular bacteria
inhibit fusion of phagosomes with lysosomes
escape into the cytosol and do not get phagocytosed
ex: mycobacterium, listeria
inhibition of class I MHC-associated antigen presentation
many viruses can do this
Block transport of antigenic peptide from cytosol to ER Removing class I MHC from ER Result in reduced class I MHC on surface
can also produce inhibitory cytokines
can directly affect the T-cells also
cell-mediated diseases and DiGeorge syndrome
Born without thymus, lack T cell component
Can fight extracellular pathogens but have
issues with intracellular pathogens (viruses, intracellular bacteria)
Th2 cells
humeral mediated immunity
Stimulate phagocyte-independent eosinophil-mediated immunity
will attack parasites
produce IL-4 (stimulation of IgE production)
produce IL-5 (activates eosinophils)
L4 and IL-13 leading to IL10 production by M2
suppresses Th1
Th17
induce inflammation
stimulate antimicrobial production: defensins
destroy extracellular bacteria and fungi
Th17 defect
bacterial abscesses and chronic mucocutaneous candidiasis
IL 17
recruit leukocytes (neutrophils)
IL-22
important in epithelial barrier integrity
Memory T lymphocytes
lymphoid organs = central memory cells
peripheral tissues = effector memory cells
require IL-7 to stay a lot
responsible for secondary response
during the immune response
survival and proliferation is maintained by antigen, CD28 co-stimulation signal, and cytokines (IL-2)
T-cell anergy
Inability of cells to proliferate in response to
engagement with MHC-peptide complex
Due to absence of appropriate costimulatory
signal or by CTLA-4 or another inhibitory signal