Cell Adaptations/Repair/Immuno Flashcards
B cells
Grow in bone marrow, involved in antibody production and memory (humoral)
T cells
Grow in thymus
Adaptive immune response
B cells are involved in the ____ immune response
Innate immunity
Humoral: Complement
Cell-mediated: phagocytes (macrophages, neutrophils, dendritic), mast, NK, basophil, eosinophil, some T cells (gamma-delta and natural killer)
Adaptive immunity
Humoral: Antibodies
Cell-mediated: B and T cells
Complement
Many different proteins circulating as inactive precursor forms, both innate and adaptive systems
Opsonization, inflammation, cell lysis
Classical complement pathway
Requires antibody/antigen complex. Part of adaptive system because specific immune response
C1 binds IgG or IgM that is bound to antigen
Lectin complement pathway
Triggered by microbial carbohydrates (MBL binds to mannose on microorganisms)
Alternate complement pathway
Microbial products directly activate complement
Opsonization
C3b binds to surface of pathogens and enhances phagocytosis (by neuts)
Inflammation from complement
C3a (and others) effect chemotaxis and mast cell degranulation resulting in histamine-mediated vasodilation and increased vascular permeability
MAC
Complement creates cell lysis when components build a tunnel through pathogen cell membrane
NK cells
Kill “irreversibly stressed” cells (infected or tumor), do not require prior exposure/activation
Minimal MHC1-self peptide, lots of NK cell-activating ligans
When stressed/abnormal, NK cells switch ratio to
Perforins/granzymes
NK cells release
Adaptive immunity cells
T cells, B cells, antigen-presenting cells
BCR (B cell receptor)
Similar to a membrane-bound antibody, targeted at a (relatively) specific antigen, can be secreted as antibodies when activated
Naive B cells
Mature, but no antigen exposure yet, Only able to express surface IgM or IgD
Plasma cells
B cell subtype, post exposure to antigen, large amounts of Ab production, apoptosis after antigens cleared
Memory cells
Long-lived B cell subtype, allow a faster response than the first time
Golgi zone
Pale zone between nucleus and cytoplasm of plasma cell, full of antibody
B-cell function
Naive cell expresses surface IgM/IgD. When receptor bound to antigen, it divides into clones, differentiates into plasma cells and memory cells
Cellular immunity
T cells need to be physically present to help and therefore are the main component of ____
Cytotoxic T cells (CD8+)
Involved in direct killing of infected cells. Detect nonself antigen being presented by infected cell **typically requires second signal
Recognizes MHC Class I
Perforin, granzyme; FAS ligand, sometimes considerable tissue damage
Cytotoxic T cells (CD8) effects
Helper T cells (CD4+)
Type of T cell that directs other immune system elements
Th1
Helper T cells that attack bacteria, recruits T cells and macrophage ?
Th2
Helper T cells that attacks parasites, recruits B cells, eos?
CD4 receptor (helper)
HIV targets _____ and then more pathogens can go unrecognized by adaptive immune system
viral illness
CD8 cells not activated leads to
Bacterial and parasitic illness
B cell class switching doesn’t happen leads to
Antigen Presenting cells (APC)
Phagocytize antigens, present antigens with MHC and activate T-cells
Often migrate to a centralized location (lymph node) to meet T cells
Dendritic cells, macrophages, B cells
Professional APCs
MHC (HLA)
Main way antigens are presented
Family of cell-surface proteins, present antigens to T cells and if its the wrong kind of antigen, T cell activation will ensure
MHC Class I
Family of cell-surface proteins, all nucleated cells have
Present whatever’s in the cell cytoplasm, usually going to be “self” antigens which won’t cause trouble, interact with cytotox T cells (CD8)
If “nonself” antigens present, I cell activation occurs
Good for intracell infections or tumors, problem in transplants, some autoimmune disorders
MHC Class II
Present on APCs, together with antigens will activate helper T cells (CD4), present phagocytized particles (present whatever APC phagocytized, not what is in cytoplasm of cell)
Recruit the inflammatory response instead of killing cell (recruit helper)
Cytokines
Proteins secreted into blood and EC fluid, communicate between cells and environment
Cytokines innate immunity
Induce inflammation, inhibit viral replication. Ex IL1, chemokines
Cytokines adaptive immunity
Lympocyte proliferation/maturation. Ex IL2, IL4, IFN-gamma, some limit or contain inflammatory process
Cytokines hematopoiesis
Increase WBC production, colony-stimulating factors
Hyperplasia
Increase in number of cells. Proliferation in response to increased demand/stim - depends on ability to synthesize DNA and divide
Hypertrophy
Increase in size of cells, no/limited capacity for division
increased synthesis of cell machinery
Atrophy
Decrease in size of cells
Metaplasia
Change to cell type better able to withstand stress
Reprogramming of stem/progenitor cells
Increase GF, GFR, cells from stem cells
Mechanisms of hyperplasia
Causes of cell injury
Hypoxia/ischemia, nutritional imbalances, physical stressor, chemical agent, infectious agent, immunologic process, genetic causes
