Peptides {hexapeptide} can have shapes similar to 20 others, so they all bind same antibody.
Muropeptides {lectin} bind to NOD, such as NOD2, and NALP intracellular receptors and trigger cytokines and/or transcription factors. Lectins include mannose-binding lectin.
Helper T cells make molecules {cytokine}| that attract neutrophils and monocytes, which become macrophages: {colony-stimulating factor} {granulocyte-macrophage colony-stimulating factor} (GMCSF) {interleukin}. Tumor necrosis factor alpha {tumor necrosis factor} increases inflammation. Inside cells, Toll-like receptors make MyD88, Mal, Tram, and/or Trif. These make NF-kappaB, which enters cell nucleus to start cytokine production. Cytokines include interleukin-1, interleukin-6, interleukin-8, interleukin-12, and tumor necrosis factor-alpha. Interleukin-1 increases inflammation. Interleukin-6 activates B cells. Interleukin-8 is signal to neutrophils. Interleukin-12 activates T cells. Cytokines attract monocytes and neutrophils. Monocytes become macrophages.
Cells inflamed by injury, allergens, antigens, or invading microorganisms release 8-kDa to 16-kDa soluble proteins {chemokine}, to attract monocytes and granulocytes. Humans have 50 chemokines.
types
Alpha chemokines have amino acids between first two cysteines and have two other cysteines. Beta chemokines have no separation between first two cysteines and have two other cysteines. Gamma chemokines have two cross-linked cysteines. Lymph nodes, lungs, liver, and bone marrow express factors {stromal-cell-derived factor 1} from genes {SDF-1 gene} {CXCL12 gene}.
receptors
Chemokines bind to chemokine receptors {G protein-linked receptor}. Chemokine receptors (CXCR2) (CXCR4) (CCR7) include chemokine receptor 5 (CCR5), used by HIV-1.
receptors: effects
Binding to receptors causes adhesion-protein {B integrin} rearrangement, to increase adhesion to blood-vessel endothelial cells. Later, leukocytes pass between endothelial cells into tissue. Leukocytes use pseudopods and actin movement to migrate along chemokine concentration gradient. High chemokine concentration makes leukocytes produce cytokines, release granule contents, induce intracellular F-actin polymerization, form pseudopods, increase endothelial and other cells, promote vascularization, remodel tissue, heal wounds, and lyse lymphocytes.
Macrophages and endothelial cells make proteins {S100 protein}, such as S100A8 and S100A9, that signal for more macrophages to come.
Tumor necrosis factor, interleukin-l, and interleukin-6 cytokines {pro-inflammatory cytokine} cause sickness responses [Maier and Watkins, 1998] [Watkins and Maier, 1999] [Watkins and Maier, 2002].
In third and fourth pharyngeal pouch, thymus helper T cells secrete peptides {lymphokine}, 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 factors, multiply helper T cells, and multiply immune precursor cells.
Helper T cells secrete lymphokine peptides, 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 {chemotactic factor}, multiply helper T cells, and multiply immune precursor cells.
T cells have cell-surface protein receptors {immunoglobulin superfamily, antibody}. These glycoproteins can have alpha, beta, gamma, and delta subunits. Receptor genes for these proteins are similar to immunoglobulin genes. They have similar constant, joining, diverse, and variable regions and similar promoters. Immunoglobulin superfamily includes cell-adhesion proteins {neural-cell adhesion molecule}, growth-factor receptors, and lymphokine receptors. MHC genes are similar to genes for antibodies and T-cell receptors.
Antibodies {abzyme} can act like enzymes and bind to reaction transition states. 10% of such binding affects reaction rates.
Immune-system B cells make one antibody type {allelic exclusion} and secrete it into blood.
One antibody arm can bind to one molecule, and other arm to another molecule {bispecific antibody}.
Variable antibody regions have only three parts that actually bind to antigen {complementarity determining region} (CDR). Variable regions otherwise just align CDRs. Humanized antibodies use human antibodies with CDRs from monoclonal mice.
Toxins can replace antibody regions {effector region} used to determine immunoglobulin type, to deliver agents only to correct sites.
Antibody variable regions can attach to different constant regions for different immunoglobulin types {class switching}, so all immunoglobulin types use same antibody.
Antibodies have two longer proteins {heavy chain}. Heavy chains have variable regions at arm ends, diverse region, joining region, and three constant regions. Single genes are for constant regions. Heavy chains can come from 20 diverse-region genes. Heavy chains can come from four joining-region genes. Thousands of genes code for variable regions. How regions bind together also varies.
Y
Two heavy chains join in middle to make Y shapes.
types
Heavy chains have five types: alpha, gamma, delta, epsilon, or mu.
antibody types
Heavy-chain type determines antibody type: immunoglobulinA or IgA, immunoglobulinG or IgG, immunoglobulinD or IgD, immunoglobulinE or IgE, or immunoglobulinM or IgM. IgA binds to antigens in saliva, tears, and intestines. IgG and IgM go into blood and bind to antigens, bound antigen binds to cells, and IgG and IgM activate immune-system macrophages, which eat cells with bound antigen. IgD are on B-cell surfaces. IgE starts mast cells that make histamine. Perhaps, histamine defends against parasites. Immunoglobulin-E can attack worms.
Antibodies have two shorter proteins {light chain}. Light chains have variable regions at arm ends, joining region, and constant region. Single genes are for constant regions. Light chains can come from five joining-region genes. Thousands of genes code for variable regions. How regions bind together also varies. Light chains parallel Y arms on outsides. Light chains have two types: kappa or lambda.
Immune-system genes rearrange in early infancy. Antibody gene can join second gene {joining gene} by deleting DNA between them. Joining genes join trunk gene, which determine mobility level. Joined genes determine antigen.
Immune-system genes rearrange in early infancy. Antibody gene can join joining gene by deleting DNA between them. Joining genes join gene series {trunk gene}, which determine mobility level. Joined genes determine antigen.
Beta2-microglobulin and other cell-surface glycoproteins {major histocompatibility protein}| (MHC) can be for cell recognition.
number
Humans can have 100,000 different surface-protein sets.
polymorphism
Cell-surface glycoproteins can be highly polymorphic.
genes
MHC genes are similar to genes for antibodies and T-cell receptors {immunoglobulin superfamily, MHC}. MHC genes do not vary through rearrangement. MHC Class I genes are expressed in all cells. MHC Class II genes make glycoproteins for B cells and macrophages. Other MHC genes make blood-complement proteins and other cell-surface proteins.
receptors
Cytotoxic T cells recognize glycoproteins.
metabolism
MHC Class I glycoproteins cut bacterial and viral antigens into peptides, which then bind to cleft in MHC Class II glycoproteins. Helper T cells recognize antigen/MHC Class II complexes. Complement proteins CD4 and CD8 bind MHC to receptors at constant antibody regions and signal T cells to activate.
T cells can have antigen receptors {T cell receptor} (TCR).
Cell-surface proteins can have classes {tissue typing}|.
Phagocyte-cell receptors {Toll-like receptor} (TLR) can recognize lipopeptides. TLR1 detects bacterial lipopeptides and parasite GPI-anchored proteins. TLR2 detects Gram-positive-bacteria cell-wall lipoteichoic acids. TLR3 detects virus double-stranded RNA. TLR4 detects Gram-negative bacteria by binding to lipopolysaccharide. TLR5 detects bacteria-flagella flagellin. TLR6 detects fungi zymosan. TLR7 detects virus single-stranded RNA. TLR8 detects virus single-stranded RNA. TLR9 detects bacterial and virus CpG sequences.
metabolism
Inside cells, TLRs make MyD88, Mal, Tram, and/or Trif. These make NF-kappaB, which enters cell nuclei to start cytokine production.
evolution
TLR are in plants and animals. Tobacco has N protein that detects tobacco mosaic virus. TLR probably started in one-celled organisms.
Outline of Knowledge Database Home Page
Description of Outline of Knowledge Database
Date Modified: 2022.0225