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20 Cards in this Set
- Front
- Back
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Lymphocyte lineage |
Hematopoietic stem cell --> common lymphoid precursor --> B cell/T-cell/NK cell |
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Granulocytes |
Neutrophils Eosinophil Basophil |
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Agranulocytes |
Macrophages Dendritic cell Monocytes |
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Types of macrophages |
M1: killer macrophages. Good at killing tumors and bacteria, produce lots of NO and antimicrobial peptides M2: healer macrophages, important for wound healing but also help tumors grow |
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Reticular macrophages |
Found on immune organs like lymph node and spleen |
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Kupffer cells |
Macrophages of the liver |
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Microglial cells |
Macrophages of the brain |
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Alveolar macrophages
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macrophages of the lungs |
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Peritoneal macrophages |
Macrophages found in the peritoneal cavity |
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Neutrophils |
Most abundant circulating leukocytes. First cells to arrive at site of injury, short lived. |
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Netosis |
Process by which neutrophils lyse themselves and throw their genetic material at a pathogen that is out of reach for them. |
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Eosinophil |
Capable of phagocytosis, specialize in destroying parasites by releasing digestive enzymes onto the parasite, causing it to die. Lives 8-12 days |
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Cells targeted by NK cells |
Virally infected Malignant Antibody coated |
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Method of cell death induction |
Receptor mediated cell death Release of toxic granules 10-18% of circulating leukocytesP |
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Perforin and granzyme |
In granules in NK cells. Perforin makes holes in the target cells, shoot granzyme into the cells and the cell has no choice but to undergo apoptosis |
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3 subsets of NK cells |
Killer (cytotoxic) Healer (tissue remodeling) IFN-g producer |
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Receptors of NK cells |
KIR are inhibitory receptors and KAR are activating receptors. MHC1 is recognized by inhibitory receptors, normal cells express MHC1 so they aren't killed. |
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3 methods of activating complement |
Alternative pathway: pathogen directly activates the complement Lectin pathway: mannose-binding lectin binds to sugar on the pathogen surface, activates complement Classical pathway: antibody mediated |
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Complement fixation |
C3 is cleaved into C3a and C3b. C3a recruits phagocytes, C3b tags the bacteria for destruction. Cleavage causes C5-9 to form membrane attack complex, allowing C9 to polymerize and form a hold in the membrane. Pokes holes in the membrane of the bacteria so it can't survive. |
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CD59 |
Protein on the surface of human cells that prevents polymerization of C9 to form pore |
