Monday - dirty d - specific acquired imunity Flashcards
X-linked agammaglobulinemia
An absence of B lymphocytes
CD40 ligand deficiency
Failure of immunoglobulin class switching
Activation-Induced Cytidine Deaminase Deficiency
Failure of immunoglobulin class switching
Common Variable Immunodeficiency
A failure to produce antibodies against particular antigens
Omenn Syndrome
VDJ recombination failure. Cannot produce BCRs or TCRs
X-linked severe combined immunodeficiency
A failure to produce mature T lymphocytes
DiGeorge syndrome
Failure of the thymus to develop correctly
Hemophagocytic lymphohistiocytosis
Failure of CD8+ T cells and NK cells to produce and/or release lytic granules
IPEX
A failure of peripheral tolerance due to defective regulatory T cells
Th1 t-cells
recognize antigen and make a lymphokine that attracts thousands of macrophages, the heavy-duty phagocytes, to the area where antigen has been recognized.
Th 17 t-cells
are similar to Th1 in that their main role is to cause focused
inflammation, although they are more powerful than Th1. They have been implicated in many serious forms of autoimmunity.
Th2 t-cells
stimulate macrophages to become ‘alternatively activated,’ able to function in walling-off pathogens and promoting healing, a process that usually takes place after the pathogen-killing Th1 response. They are very important in parasite immunity.
Follicular Helper T cells, Tfh
are stimulated by antigen and migrate from T cell areas of lymph nodes into the B cell follicles, where they help B cells get activated and make the IgM, IgG, IgE and IgA antibody subclasses.
Regulatory T cells, Treg
make cytokines that suppress the activation and function of Th1,
Th17, and Th2 cells, so they keep the immune response in check. They are part of the Th family. Ipex is a disease where these aren’t working properly.
Cytotoxic or killer T cells, CTL
destroy any body cell they identify as bearing a
foreign or abnormal antigen on its surface.
