This is a Twitter summary from the 2018 WSAAI meeting. This summary was compiled from the tweets posted by @MatthewBowdish, an allergist/immunologist, who attended the 2018 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited and modified by me.
Larry Borish "Mast cells: How did such nice cells get such a bad reputation?"
Mast cells in evolution: https://twitter.com/MatthewBowdish/status/955499705324126208
Role of mast cells in immunity: homeostasis (wound repair, revascularization), Infxn (bacteria, protozoans, helminths), Envenomation, When Good Cells Go Bad (allergies, anaphylaxis).
Anti-FceR1 autoantibodies in chronic autoimmune urticaria: IgG against FceRI (receptor for IgE) (click to enlarge the image).
Why is there histamine? No clinical use due to its adverse effects (mucus production, congestion, n/v/cramps/diarrhea, low BP). Name a condition for which we order "a unit" of IV histamine STAT from the pharmacy? And why are there cysteinyl leukotrienes? Proteases? Tryptase? Most of these mediators lead to common "themes," vascular leakage and vasodilation.
Why is there tryptase? https://twitter.com/MatthewBowdish/status/955503469468643328
Mechanisms of Mast Cell Activation are much more diverse than IgE alone: https://twitter.com/MatthewBowdish/status/955504187390902272
IgE activation of mast cells is an after thought of evolution, coming 230 million years after mast cells appear.
Dr. Borish believes "sick building syndrome" is real and you don't need a positive skin test (ie IgE-activation). Likely due to pathogen-associated molecular patterns (PAMP) pathways for organisms like Alternaria - Bankova LG et al Proc Natl Acad Sci 2016).
sPLA2-X in EIB: https://twitter.com/MatthewBowdish/status/955506332118933509
sPLA2-X closely resembles Bee Venom PLA2. Why is this interesting? Because getting stung by a bee is one of the best diagnostic tests for mastocytosis, and this explains why mastocytosis pts can react to bee venom and have neg skin/blood tests to venom IgE.
So why again is there histamine? Short answer-you cannot have an immune response if acute phase proteins (complement, antimicrobial proteins) or inflammatory cells (neutrophils, wound healing) can't get out of the circulation and can't migrate through tissue matrix. Example of this is local IgE to venoms will promote - local- mast cell degranulation and neutralize the toxin - locally - before it gets into the circulation.
Matthew Bowdish MD @MatthewBowdish: I asked Larry Borish about other mediators to measure than serum tryptase. He mentioned two, one practical (urine for prostaglandin D2) and the other impractical (PAF - prob most sensitive blood test but not clinically available).
Larry Borish "Mast cells: How did such nice cells get such a bad reputation?"
Mast cells in evolution: https://twitter.com/MatthewBowdish/status/955499705324126208
Role of mast cells in immunity: homeostasis (wound repair, revascularization), Infxn (bacteria, protozoans, helminths), Envenomation, When Good Cells Go Bad (allergies, anaphylaxis).
Anti-FceR1 autoantibodies in chronic autoimmune urticaria: IgG against FceRI (receptor for IgE) (click to enlarge the image).
Why is there histamine? No clinical use due to its adverse effects (mucus production, congestion, n/v/cramps/diarrhea, low BP). Name a condition for which we order "a unit" of IV histamine STAT from the pharmacy? And why are there cysteinyl leukotrienes? Proteases? Tryptase? Most of these mediators lead to common "themes," vascular leakage and vasodilation.
Why is there tryptase? https://twitter.com/MatthewBowdish/status/955503469468643328
Mechanisms of Mast Cell Activation are much more diverse than IgE alone: https://twitter.com/MatthewBowdish/status/955504187390902272
IgE activation of mast cells is an after thought of evolution, coming 230 million years after mast cells appear.
Dr. Borish believes "sick building syndrome" is real and you don't need a positive skin test (ie IgE-activation). Likely due to pathogen-associated molecular patterns (PAMP) pathways for organisms like Alternaria - Bankova LG et al Proc Natl Acad Sci 2016).
sPLA2-X in EIB: https://twitter.com/MatthewBowdish/status/955506332118933509
sPLA2-X closely resembles Bee Venom PLA2. Why is this interesting? Because getting stung by a bee is one of the best diagnostic tests for mastocytosis, and this explains why mastocytosis pts can react to bee venom and have neg skin/blood tests to venom IgE.
So why again is there histamine? Short answer-you cannot have an immune response if acute phase proteins (complement, antimicrobial proteins) or inflammatory cells (neutrophils, wound healing) can't get out of the circulation and can't migrate through tissue matrix. Example of this is local IgE to venoms will promote - local- mast cell degranulation and neutralize the toxin - locally - before it gets into the circulation.
Matthew Bowdish MD @MatthewBowdish: I asked Larry Borish about other mediators to measure than serum tryptase. He mentioned two, one practical (urine for prostaglandin D2) and the other impractical (PAF - prob most sensitive blood test but not clinically available).