This blog post may change. It looks as if il-3 behaves like il-6 in converting B cells into plasma cells.
il-3 and il-6
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189411/
https://www.researchgate.net/publication/20372389_Human_recombinant_IL-3_stimulates_B_cell_differentiation
il-3 produced by skin matured mast cells when they see viruses would stimulate the B cells to become plasma cells after they interact with TH1 or TC producing IgG2 or IgG3.
il-6 stimulates B cells to start producing IgM when a visible infection was seen. The B cells then interact with Follicular dendritic cells or langerhans to produce IgA IgE or IgG1.
The cytosol antigens involve the TH1-B cells and would have IFN gamma producing IgG2 instead of il-4. The mito/nuclear antigens would involve Tc-B cells and il-10 producing IgG3.
il-5 validates that it is not a tumor growing due to a viral infection causing cancer?
Note that gm-csf is also released by TH17 after the vacuole or inner organelle is popped.
outer antibodies and B cells: insulin IgG1 spleen, GH IgA peyer patches , IGF-1 IgE lymph
Two types of human mast cells
http://www.pnas.org/content/83/12/4464?ijkey=0c1e165e66f17fb90b06151a9409ad54cba6eae9&keytype2=tf_ipsecsha
Skin derived and Bone derived mast cells
https://www.ncbi.nlm.nih.gov/pubmed/15214039
https://www.ncbi.nlm.nih.gov/pubmed/15210814
TLR 3 Golgi
TLR7 Nucleus
TLR9 mitochondria
Eosinophils to divide into 3 groups if you look at chemokine receptors
the cytosol antigens TH1 pathways
cxcr3 and eosinophils
https://www.ncbi.nlm.nih.gov/pubmed/10903763
the nuclear/mitochondria antigens Tc pathways
cxcr4 and eosinophils
https://www.ncbi.nlm.nih.gov/pubmed/10820276
the outer antigens TH2 pathways
ccr3 and eosinophils
https://www.ncbi.nlm.nih.gov/pubmed/12496441
il-3 and IgE receptors on Mast cells (binding of IgE decreases il-3)
https://onlinelibrary.wiley.com/doi/pdf/10.1002/1521-4141%28200208%2932%3A8%3C2308%3A%3AAID-IMMU2308%3E3.0.CO%3B2-X
il-3 decreases IgE antibodies
https://www.ncbi.nlm.nih.gov/pubmed/458056
https://www.ncbi.nlm.nih.gov/pubmed/80144
IL-3 were found to release more histamine and LTC4 but not PGD2
PGD2 is involved with microbial infections
Leukotrienes type LTC4 elevated in viral infections
https://www.ncbi.nlm.nih.gov/pubmed/14533659
Staph infections appear to evade detection and destruction by confusing the immune system. The trigger of leukotrienes makes it look like a viral infection is occurring.
Staphylcoccous aureus' enterotoxins induce leukotrienes
https://www.ncbi.nlm.nih.gov/pubmed/11531797
LTB4 acts against mycobacteria
http://journals.sagepub.com/doi/pdf/10.1177/000456329703400205
5-HETES becomes LTC4 or LTB4
gm-csf from il-23 stimulated TH17
https://www.nature.com/articles/ni.2044
il-3 and il-6
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189411/
https://www.researchgate.net/publication/20372389_Human_recombinant_IL-3_stimulates_B_cell_differentiation
il-3 produced by skin matured mast cells when they see viruses would stimulate the B cells to become plasma cells after they interact with TH1 or TC producing IgG2 or IgG3.
il-6 stimulates B cells to start producing IgM when a visible infection was seen. The B cells then interact with Follicular dendritic cells or langerhans to produce IgA IgE or IgG1.
il-5 validates that it is not a tumor growing due to a viral infection causing cancer?
Note that gm-csf is also released by TH17 after the vacuole or inner organelle is popped.
outer antibodies and B cells: insulin IgG1 spleen, GH IgA peyer patches , IGF-1 IgE lymph
http://www.pnas.org/content/83/12/4464?ijkey=0c1e165e66f17fb90b06151a9409ad54cba6eae9&keytype2=tf_ipsecsha
Skin derived and Bone derived mast cells
https://www.ncbi.nlm.nih.gov/pubmed/15214039
https://www.ncbi.nlm.nih.gov/pubmed/15210814
TLR 3 Golgi
TLR7 Nucleus
TLR9 mitochondria
Eosinophils to divide into 3 groups if you look at chemokine receptors
the cytosol antigens TH1 pathways
cxcr3 and eosinophils
https://www.ncbi.nlm.nih.gov/pubmed/10903763
the nuclear/mitochondria antigens Tc pathways
cxcr4 and eosinophils
https://www.ncbi.nlm.nih.gov/pubmed/10820276
the outer antigens TH2 pathways
ccr3 and eosinophils
https://www.ncbi.nlm.nih.gov/pubmed/12496441
il-3 and IgE receptors on Mast cells (binding of IgE decreases il-3)
https://onlinelibrary.wiley.com/doi/pdf/10.1002/1521-4141%28200208%2932%3A8%3C2308%3A%3AAID-IMMU2308%3E3.0.CO%3B2-X
il-3 decreases IgE antibodies
https://www.ncbi.nlm.nih.gov/pubmed/458056
https://www.ncbi.nlm.nih.gov/pubmed/80144
IL-3 were found to release more histamine and LTC4 but not PGD2
PGD2 is involved with microbial infections
Leukotrienes type LTC4 elevated in viral infections
https://www.ncbi.nlm.nih.gov/pubmed/14533659
Staph infections appear to evade detection and destruction by confusing the immune system. The trigger of leukotrienes makes it look like a viral infection is occurring.
Staphylcoccous aureus' enterotoxins induce leukotrienes
https://www.ncbi.nlm.nih.gov/pubmed/11531797
LTB4 acts against mycobacteria
http://journals.sagepub.com/doi/pdf/10.1177/000456329703400205
5-HETES becomes LTC4 or LTB4
gm-csf from il-23 stimulated TH17
https://www.nature.com/articles/ni.2044
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