Autoimmunity and mast cells.


A13
7mo ago by MyPatientMatch User

.Also how histadine becomes histamine. Plus kinases.

"Aberrant kinase activity is implicated in an increasing number of diseases, with more than 400 human diseases now linked either directly or indirectly to protein kinases." (Repeated and referenced later.)

T cell / B cells have to get mast cells involved in autoimmune inflammation, before innate immune cells are ever engaged in the autoimmune process.

Mast cells are part of the innate immune systems. T and B cells are part of the adaptive system.

Longer version with Paragraphs Rearranged.

"While the adaptive immune response [T and B cells] initiates autoimmune inflammation, innate immune cells are critical for sustaining the response that leads to pathology (reviewed in Bach et al., 2004; Tenner, 2004; Marshak-Rothstein and Ohashi, 2007; Pisetsky, 2008; Chervonsky, 2009; Maciejewska Rodrigues et al., 2009).

"...However, by definition, mast cells can only act as accessory cells to the self-reactive T and/or antibody driven autoimmune responses. Thus, when evaluating mast cell involvement using existing and somewhat imperfect animal models of disease, their importance is sometimes obscured. However, these potent immune cells are undoubtedly major contributors to autoimmunity and should be considered as important targets for therapeutic disease intervention.

"...By definition, the directors of autoimmune responses are cells of the adaptive immune system. Thus, an early event in the development of autoimmunity is the activation and expansion of T and/or antibody-producing B cells bearing self molecule-reactive receptors.

"Naive autoreactive T or B cells first encounter antigen in secondary lymphoid organs where they undergo differentiation and acquire their effector function. These primed CD4+ T helper cells, CD8+ T cytolytic cells or secreted antibody molecules enter the blood stream and migrate to sites of inflamed tissues expressing relevant autoantigens (Figure (Figure1).1).

"T cells, through the elaboration of cytotoxic mediators, and antibodies, through complement fixation or their ability to activate resident accessory cells such as macrophages and mast cells via Fc receptor engagement, can play direct roles in tissue destruction at these sites (Lohr et al., 2005).

Title:
Mast Cells are Important Modifiers of Autoimmune Disease: With so Much Evidence, Why is There Still Controversy?
Melissa A. Brown and Julianne K. Hatfield
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369183/

3 Save

A13
7mo ago by MyPatientMatch User

Prep work for next study.
How histadine becomes histamine. Short version, it gets phophorylated.A phosphate is attached.

Histadine decarboxylase/HDC is an enzyme responsible for catalyzing the decarboxylation of histidine to form histamine. The sole member of the histamine synthesis pathway, producing histamine in a one-step reaction. Histamine cannot be generated by any other known enzyme.

HDC is therefore the primary source of histamine in most mammals and eukaryotes. The enzyme employs a pyridoxal 5'-phosphate (PLP) cofactor, in similarity to many amino aciddecarboxylases.

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A13
7mo ago by MyPatientMatch User

tle
Reversible phosphorylation of histidine residues in proteins from vertebrates.
Klumpp S1, Krieglstein J.
https://www.ncbi.nlm.nih.gov/pubmed/19278958

Signaling by kinases and phosphatases that act on serine, threonine, and tyrosine residues of proteins is among the most extensively studied regulatory mechanisms in mammalian cells, and research focused in this area is ongoing.

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