B cells and T cells make antibodies against antigens {adaptive immune system}.
T cells can phagocytize foreign cells and viruses {cell-mediated system} {cellular immunity}|. After contacting cells having different MHC surface proteins, lymphocytes change to macrophages, as antigen combines with special RNA, which engulf foreign cells. Memory cells take information back to lymph nodes and spleen, where memory cells change to plasma cells.
Immune system can kill bacteria and viruses in cell fluids {humoral immunity}| {humoral system}. Plasma cells make 2000 antibodies per second for several days to prevent reinfection.
The first time {primary immune response} bodies react to new antigens has greatest reaction {immune response}|. Later antigens cause reactions {secondary immune response}.
Natural killer cells can attach to B cells at temporary synapses {immune synapse}, to check if they are functioning. Natural-killer-cell receptor proteins check B-cell surface proteins. If no reception, acidic organelles move to synapse and inject chemicals to kill cells. Antigen-presenting cells contact T cells {supramolecular activation cluster, immunity} at immune synapses to present protein fragments that they removed from viruses or bacteria and activate T cells. Immune-synapse outer ring is for adhesion, and central spot is for recognition. Proteins move to form patterns, using cytoskeletons.
Body cells can react to pathogens {innate immune system}.
cells
Phagocytes include monocytes and dendritic cells. Monocytes become macrophages.
receptors
Pathogen molecules cause inflammation. Phagocyte Toll-like receptors recognize molecule types.
cytokines
Inside cells, TLRs make MyD88, Mal, Tram, and/or Trif. These make NF-kappaB, which enters cell nucleus to start cytokine production.
dendritic cells
After phage ingestion, dendritic cells carry phage fragments to lymph nodes to inform T cells.
Spleen, lymph nodes, liver, and bone marrow blood-vessel sinusoid cells phagocytize foreign cells {reticuloendothelial system}.
Immune system has rapid generalized responses {sickness response}| {acute phase response}.
purpose
Sickness response creates or saves energy.
process
Stress causes hypothalamus, pituitary, adrenal gland, and sympathetic nervous system to release hormones and transmitters, which bind to immune-cell receptors and regulate immunity. Activated immune cells release pro-inflammatory cytokines that affect neurons and glia, which coordinate hormone, behavior, and physiological changes related to fever. Physiological changes are fever, blood-ion-concentration reduction, increased white-blood-cell replication, and increased sleep. Blood-ion-concentration reduction denies minerals required by replicating bacteria and viruses. Behavior changes decrease social interaction, exploration, sexual activity, and food and water intake. Hormone changes increase hypothalamus, pituitary, adrenal, and sympathetic-nervous-system hormone release.
fever
Fever raises body temperature, so bacteria and viruses do not replicate rapidly, bacteria do not form protective outer coats, white blood cells replicate rapidly, and destructive enzymes function efficiently.
slow response
Immune system has slow selective response, which makes antibodies [Maier et al., 1994] [Maier and Watkins, 1998] [Maier and Watkins, 2000].
glia
Glia can act like immune cells.
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Date Modified: 2022.0225