--APC = antigen presenting cell, professional, these have MHC-II pathway and include macrophages and DC's
--B220 on B cell makes IgM, D, G, E, A, evolved with T cells (same as CD-45)
--CD1 is on almost all cells, definitely all epithelium, presents fats and sugars so T cells can respond to non-proteins
--CD3 is next to TCR on T cells, is phosphyrlated when T cell hits MHC
--CD4 on "helper" T cells
--CD4+CD25+ = active Treg, suppress T cells via
--CD4 and CD8 T cells in the gut both make TGFβ
--CD4 Th1 cells activate infected macrophages, help B cells make Ab's, target microbes that persist in macrophage vesicles (mycobacteria, Listeria, Leishmania, donovani, Penumocystis carinii) and extracellular bacteria
--CD4 Th2 cells help B cells make Ab, esp IgE to target helminth parasites
--CD4 Th17 cells ENHANCE NETROPHIL RESPONSE and target extracellular bacteria (Salmonella)
--CD5 is an ancient B cell, located in mucosal tissue, makes IgM only
--CD4 Treg cells suppress T cell responses
--CD8 "killer" or cytotoxic T cells kill virus-infected cells (flu, rabies, vaccinia) and some intracellular bacteria (use perforin)
--CD8's <-- activated by Th1 CD4's via cytokine ( ??? name it )
--CD34 is on all stem cells that will become immune cells
--CD40 is costimulatory
--CD40L = matches costimulatory on T cell, switches B cells to next class
--CD45 marks regular B cell that makes all kinds of antibodies
--CD80 is a costimulatory signal
--CD86 is costimulatory, the biggie that you find on APC's
--DC = dendritic cell
--Fc alpha is anti-inflam
--FCD = follicular dendritic cell, not related to dendritic cell
--GM-CSF = granulocyte monocyte colony stimulating factor, granulocyte proliferation, mast cells, macrophages
--IFNγ --> pro-inflam, reduces susceptibility to virus
--IFNγ --> Th1 response to bacteria, viruses, cancer
--IFNγ --> decreases IL-4, increases macrophages, ROS, phagocytosis
--IFNγ --> B cells class switch to IgG
--IFNγ --> activates CD8 T cells, increases perforin & granzyme production
--IgA (mucosal) <-- Th3
--IgE <-- Th2
--IgG <-- Th1
--IL-1 --> fever, sleepiness, proinflam with IL-6
--IL-1 is good for acute infx and leads to depression if there's no infx to fix
--IL-1 <--adipose, resistin
--IL-2 --> proliferation of T cells, all kinds including naive, B cells switch to IgM
--IL-4 --> Th2 --> IL-4, 5, 10, 13, B cells class switch to IgE, lowers IFNγ
--IL-4 inhibits Th3 response
--IL-5 is part of Th2 response, sensitizes mast cells, B cells class switch to IgA
--IL-6 is pro-inflam, adipokine, does not inhibit Th3 response
--IL-6 --> increased circulation, acute inflammation, osteoblasts say make osteoclasts
--IL-6 --> anxiety, increases with panic and stays high longer in females
--IL-6 --> increases cortisol, increased during intense exercise, muscle contraction
--IL-7 <--made by macrophages and DC's
--IL-7 is the default growth cytokine for undifferentiated Th0 proliferation --> IL-2
--IL-8 <-- from adiopose, visfatin
--IL-8 is a chemokine that brings neutrophils especially to adipose tissue
--IL-10 --> Th3 response, decreases Th1, increases Th2
--IL-12 --> activates Th1 --> IFNgamma, GM-CSF, TNFalpha, IL-2, more IL-12,
--IL-12 --> B cells class switch to IgG
--IL-12 <-- decreased by stress
--IL-12 <-- made by DC and macrophages
--IL-12 inhibits Th3 response
--IL-13 is part of Th2 response and causes mucus production
--IL-15 more in gut
--IL-17 --> activates Th17 -->more IL-17, but NOT IL-4 or IFNγ
--IL-17 --> stimulates neutrophils, regulates chemokine production
--IL-23-->division of Th17 (fungus can increase production of IL-23 in place of IL-12)
--IL-23, (TGFβ, IL-6) --> Th17
--TGFβ --> activates Th3 --> IL-10, CD4+CD25+ Th3 cells, IL-2, →IgA class switch, inhibits B cell and macrophage growth
--TGFβ --> B cells class switch to IgA
--TGFβ in the gut made by both CD4 and CD8 T cells
--TGFβ enhances differentiation of other Th3 cells
--TGFβ downregulates production of IL-12 by DCs and macrophages (downreg Th1)
--TGFβ, IL-6, IL-23 --> Th17
--TNFalpha -- too much causes leaky gut, Crohn's, Ulcerative colitis (IgG vs enteric microbes, colon too acidic)
--TNFalpha --> increase macrophage ROS, brings in lymphocytes, macs, eos basos
--TNFalpha -- burn victims make so much they don't get cancer
--TNFalpha <-- made by macrophages and DC's, adipose too, part of Th1 response
--Th0 = naive
--Th1 --> IFNγ, GM-CSF, TNFalpha, IL-2, more IL-12, class switch to IgG
--Th2 --> IL-4, 5, 10, 13, class switch to IgE-->eos & mast degranulation, diarrhea
--Th3 --> IL-10, CD4+CD25+ Th3 cells, IL-2, →IgA class switch, inhibits B cell and macrophage growth
--Th17 <-- HIV pts are deficient in these cells
--Th17 -->more IL-17, but NOT IL-4 or IFNg (inhibited by IL-4, 12)(OK with IL-6 and TGFb)
--Th17 express receptors for IL-23-->increased division
--Th17 --> stimulates neutrophils, regulates chemokine production (HIV patients are deficient in Th17 cells)
--Th17 --> IL-17, IL-6 --> acute inflammation, autoimmunity??
--TLRs less in gut, some bact in gut don't bind TLR's anymore
--Treg <-- activated by TGFβ ?? Th3 tolerance