Humoral immunity uses immune-system cells {macrophage}| that find antigens and process them.
Precursor cells {hemopoietic stem cell} (HSC), trapped inside bone-marrow special-cell {stromal cell} pockets, make all immune-system cells.
Hemopoietic stem cells divide to make cells {multipotent progenitor cell} (MPP) that move out of stroma and make hemopoietic stem cells that stay in stroma. Multipotent progenitor cells divide into myeloid progenitors and lymphoid progenitors. Myeloid progenitors divide into granulocytic/monocytic precursors and megakaryocytic/erythrocytic precursors. Lymphoid progenitors divide into B-cell precursors and T-cell precursors.
Mammalian immune-system bone-marrow cells {B cell}| synthesize and secrete antibodies and migrate to spleen, liver, and lymph nodes. If antigens meet B cells with correct antibodies, B cells transform into plasma cells.
antibodies
B cells differentiate from making IgM to making IgG to making IgA. B cells transpose variable region, located far from constant-region gene, to joining region, to make different antibodies. Enhancer activates only one variable-gene promoter. Vertebrate immune-system B cells use controlled transposition to make one antibody. Antibodies have constant regions. Various joining regions can attach to constant region. Various variable regions, located far from constant region in genome, can transpose to joining region.
Cells {memory cell} can take information back to lymph nodes or spleen, where memory cells change to plasma cells.
Cells {plasma cell}| can come from B cells. Plasma cells are lymphocytes that make antibodies and bind to foreign proteins. They make only one antibody type, which reacts with antigen to form precipitates for phagocytization. Humoral system makes 2000 antibodies per second for several days to prevent re-infection. Immature plasma cells in fetus that make antibodies against self normally die, leaving only antibodies against foreign molecules at birth.
IgD are on B-cell surfaces. IgE starts cells {mast cell}| that make histamine.
Immune-system cells {natural killer cell} can attach to B cells at temporary synapses to check if they are functioning.
In third and fourth pharyngeal pouch, thymus immune-system cells {T cell}| produce lymphokines from precursors. T cells can phagocytize foreign cells and viruses {cellular immunity, T cell}. Cytotoxic T cells absorb damaged cells.
cell surface
T cells have surface protein receptors. These glycoproteins can have alpha, beta, gamma, and delta subunits. Receptor genes for these proteins are similar to immunoglobulin genes. Immunoglobulin superfamily has similar constant, joining, diverse, and variable regions and similar promoters.
T cells {CD4+ T lymphocyte} {helper T cell} can have cell-surface CD4-protein receptors {co-receptor}, which assist T-cell receptors. Helper T cells have T-cell receptors.
process
Helper T cells start disease-organism killing. Helper T cells secrete lymphokines, such as interleukin, interferon, colony-stimulating factor, and tumor necrosis factor. Lymphokines activate cytotoxic T cells, signal B cells to make antibodies, attract macrophages and platelets with chemotactic factor, multiply helper T cells, and multiply immune precursor cells.
regulatory T cells
5% to 10% of helper T cells have CD25 surface protein and Foxp3 transcription factor and inhibit autoreactive CD4+ T lymphocytes.
problems
CD4+ T lymphocytes can alter to cause multiple sclerosis, insulin-dependent diabetes of youth, and rheumatoid arthritis.
Helper T cells {regulatory T cell} {CD4+CD25+ T cell} {T-reg cell} {T regulatory cell} can inhibit helper-T-cell immune responses, rather than secrete cytokines or engulf infected cells. 5% to 10% of CD4+ T lymphocytes are regulatory T cells.
receptors
Regulatory T cells have T-cell receptors, CD4-protein receptors, and CD25 surface proteins, which are in interleukin-2 receptors. Interleukin-2 excites regulatory T cells.
transcription
They have Foxp3 transcription-factor protein, which makes molecules that can disable autoreactive T cells.
Perhaps, antigen-specific receptors are stronger than the ones for autoreactive CD4+ T lymphocytes. Perhaps, regulatory T cells inhibit antigen-presenting cells from showing antigen. Perhaps, regulatory T cells cause antigen-presenting cells to release inhibitory cytokines. Perhaps, regulatory T cells inhibit autoreactive CD4+ T lymphocytes directly.
problems
Foxp3-gene mutation can cause immune dysregulation polyendocrinopathy enteropathy X-linked chromosome syndrome {IPEX syndrome} and autoreactive immune systems. Scurfy mice have autoreactive immune systems.
T cells {dendritic cell} can have surface molecules that bind to non-self proteins and attract T cells to breakdown protein. Then they usually die.
Cells {antigen-presenting cell} can contact T cells, to present protein fragments {supramolecular activation cluster, antigen} that they removed from viruses or bacteria, and so activate T cells. Supramolecular-activation clusters have outer rings for adhesion and central spots for recognition. Proteins move to form patterns, using cytoskeletons.
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Date Modified: 2022.0225