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Final Exam

Neutralization *Ab binds to Ag to keep it from entering host cell→ phagocytosed and eliminated *Discourages/prevents Ag from initiating an infection
Opsonization Ab coats Ag→ Fc Receptors on phagocyte bind Ab→ Ag undergoes phagocytosis→ Ag is eliminated
Thymus-dependent antigen Ag broken down→ MHC2 presents Ag peptide on cell surface→ Helper T cell recognize Ag→ TCR binds to MHC2 and activates T cell→ T cell stimulates B cells to become plasma cells
Thymus-independent antigen Independent antigen → no T-cell coming to help Just right amount of epitopes on surface that B-cell receptors can bind, Too much epitope causes them to die from anergy, Signal 2 not really needed
B-cell Co-receptors (CD19, CD21, CD81) Binding of CD21 to C3dg-tagged antigens allows the co-receptor to cluster with the Ag receptor → co-ligation of the co-receptor allows receptor-associated kinases to phosphorylate CD19 →
co-receptors continued... phosphorylated CD19 binds Src-family tyrosine kinases and PI 3-kinases → PI 3-kinases cascades and activates B-cell.
Linked Recognition A given B-cell can only be activated by helper T-cells that respond to the same Ag.
Linked Recognition Process B-cell binds virus through viral coat protein→ Virus particle is internalized and degraded→ peptides from internal proteins of the virus are presented to the T-cell, which activates the B-cell (helper T-cell, CD40 and CD40L, cytokines) →
last step on linked recognition process activated B-cell produces antibody against viral coat protein.
Cognate T-cell A helper T-cell primed by the same Ag depends on the ability of the Ag specific B-cell to concentrate the appropriate peptide on its surface MHC II
CD40L/CD40 Bidirectional Stimulation Binding of CD40 and CD40L helps to drive the resting B-cell into the cell cycle and is essential for B-cell responses to thymus-dependent Ags.
CD40L/CD40 Bidirectional Stimulation process T-cell receptor binds Ag presented by B-cell → CD40L is induced on the T-cell→ this then binds to CD40 on the B-cell→ Integrin LFA-1 on the T-cell interacts with the adhesion molecule ICAM-1 on the B-cell →
last step of CD40L/CD40 cytoskeleton protein talin is reoriented by the cytoskeleton toward the point of contact with the B-cell.
Primary focus Initial area of differentiating B-cells that forms outside the follicles in peripheral lymphoid tissues after Ag activation.
Primary lymphoid follicle B-cell areas or B-cell zone Aggregates of resting B lymphocytes in peripheral lymphoid organs.
Secondary lymphoid follicle Follicles with germinal centers. A follicle containing a germinal center of proliferating activated B-cells during an ongoing adaptive immune response
Mantle Zone Outer layer of resting B-cell Germinal center→ mantle→ dark zone→ light zone A rim of B lymphocytes that surrounds lymphoid follicles.
Dark Zone Where centroblast reside or are growing and generates B-cells
Follicular dendritic cell Within the follicle, the follicular dendritic cell secrete CXCL13 while naive cells B cells express CXCR5, the receptor for this chemokine.
Plasmablasts A b-cell in a lymph node that already shows some features of a plasma cell
Plasmablasts process B-cell activation→ plasmablast → 1st focus Migrate to the germinal center Becomes centroblast
Centroblasts B-cells in the germinal center proliferate, dividing every 6-8 hours Rapidly proliferating B-cells Expresses chemokine receptors CXCR4 and CXCR5 Markedly reduce their expression of surface immunoglobulin particularly of IgD
Cyclic Reentry Model of the dynamics of b-cell migration within the germinal center The back and forth movement of cells in the
Affinity Maturation The affinity and specificity of positively selected B-cells are continually refined during the germinal center response
Fc Receptor Facilitate the phagocytosis of Ab-bound extracellular pathogens by macrophages, DC, and neutrophils.
When Fc receptors of nonphagocytic cells are engaged by Ab-coated pathogens... the NK cells, eosinophils, basophils, and mast cells are triggered to secrete stored mediators.
primary immune response several days are required for the clonal expansion and differentiation of naive lymphocytes into effector T-cells and Ab-secreting B-cells Occurs against a pathogen encountered for the first time.
Secondary Immune response Immune response that occurs in response to a second exposure to an antigen Starts sooner, produces greater levels of antibodies Produces class-switched antibodies\generated by the reactivation of memory lymphocytes
Tertiary Immune response adaptive immune response
Immunological Memory It ensures a rapid reinduction of Ag-specific Ab and effector T cells on subsequent encounters with the same pathogen, thus providing long lasting and often lifelong protection against it.
Homing Receptors Adhesion molecules Receptors on lymphocytes for chemokines, cytokines, and adhesion molecules specific to particular tissues, and which enable the lymphocyte to enter that tissue.
CLA Glycosylated isoform of PSGL-1 that binds to E-selectin on cutaneous vascular endothelium CLA-expressing T lymphocytes also produce the chemokine receptor CCR4. This binds CCL17
CLA process Interaction btwn CLA with E-selectin causes the T-cell to roll against the wall of the blood vessel → signal delivered by endothelial CCL17 → causes the arrest of lymphocytes and brings about adhesion to the wall.
CCR4 Specific to naive T cells Chemokine receptor produced by CLA-expressing T-lymphocytes responds to chemokines secreted by epithelial cells like CCL17 homes T-cells into epithelium
CCR4 process Binds the chemokine CCL17 (TARC) Present at high levels on the endothelium of cutaneous blood vessels Signal delivered by endothelial CCL17 is thought to cause the arrest of lymphocytes and to bring about their adhesion to the vessel wall
CXCR4 Centroblasts expresses CXCR4, which keeps that B-cell in that B-cell zone, homes them into the dark zone
CD45RA expressed by B-cells, T-cell subsets (naive T-cells), monocytes Isoform of CD45 containing the A exon RA is expressed by naive T-cells
CD45RO lowers threshold response of effector T cells ...expressed on T-cell subsets, B-cell subsets, monocytes, macrophages Isoform of CD45 containing none of the A,B,C exons RO expressed by effector t-cells
PSGL-1 Expressed by activated T-cells Binds to P-selectin on endothelial cells via adhesive interactions Allows for T-cells to enter all tissues in very small numbers
Memory Cells Long-lived lymphocyte capable of responding to a particular Ag on its reintroduction long after the exposure that prompted its production Self-renew Protect against infection
Effector Memory Able to respond quickly and create effector cells cytotoxic → CD8....TH1, TH2, etc. → CD4 Long-lived CCR7 not found in effector cells
Central Memory Slow at becoming effector cells Longest-lived CCR7 expressed in high level
Antigenic Drift Mechanism for variation in virus that involves the accumulation of mutations w/in genes that encode for Ab-binding sites slight changes due to point mutations, partial protection due to it only being a slight change
Cause of Antigenic Drift Caused by point mutations in the genes encoding hemagglutinin and a second surface protein, neuraminidase (for influenza) Allows for new variants of the flu virus to arise within populations that are already immune to previous variations
Antigenic Shift genetic material being swapped by secondary host. when infected by it again there is no protection at all.
Antigenic Variation Mechanism where infectious organism alters surface protein to avoid being killed by immune response Different type of same pathogen, changes in antigenic type shift and drift, programmed gene rearrangement
Serotypes Different types of pathogens are distinguished by using specific antibodies as reagents in serological tests Infection with one serotype can lead to a type-specific immunity Groups of cells distinguished by shared cell surface Ag such as IgG1 IgG2 etc.
Latency Ability for pathogenic virus to lie dormant w/in a cell The virus is not being replicated and does not cause disease However, because there are no viral peptides to signal its presence, it cannot be eliminated
Herpes simplex virus (HSV) = HHV1 and HHV2 Causes cold sores which infects epithelial cells and spreads to neurons serving the infected area Effective immune response can control the cold sores in the epithelial cells but the virus persists in a latent state in the sensory neurons
HHV-3 -- herpes zoster Causes chickenpox Remains latent in one or a few dorsal root ganglia after the acute illness is over Can be reactivated by stress or immunosuppression
HHV-4 -- EBV (epstein barr virus) infect B-cells and kills most, remaining become long lived B-cells Transforms B-cells, Immortalizes cell → can lead to cancer cells T-cells prevent this from happening monocytes EBNA-1 down regulates TAP = less MHC expression
HHV-5 -- CMV CMV known for chronic reinfections --> more T-cells dedicated to fight CMV 30-50% of immune cells respond to CMV Leaves host open to other infections CMV makes its own IL-10 to shut down immune response Changes the whole subset of T-cells responding
IF EBV give you mono and can transform B-cells which can lead to cancer. How come you don't get cancer every time you have mono? the T-cells and NK cells keep them in check and kill all the transformed B-cells
Created by: cgalici1



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