CD4(+) T cells were activated during the onset of OA, but cartilage damage was more prominent at a later stage. CD4(+) T cells were involved in the pathogenesis of OA: they induced MIP-1γ expression and subsequent osteoclast formation.

Thrombocytopenia as well as hemoconcentration and leukopenia followed by leukocytosis were induced after HoGG challenge on HoGG-sensitized mice. Thrombocytopenia was induced within 2 min and sustained for 1 day. HoGG-induced thrombocytopenia was not observed until day 10 after sensitization; mice challenged with HoGG dose > or = 10 micrograms developed thrombocytopenia. Two types of thrombocytopenia were observed in appropriately sensitized mice. HoGG induced thrombocytopenia at 2 min and 60 min, whereas, alpha-macroglobulin induced thrombocytopenia at 2 min, the platelet count of which returned to normal within 60 min. Poly (Glu60Ala30Tyr10) did not induce thrombocytopenia at 2 min or 60 min. The tracing study by 3H-serotonin labelled platelets demonstrated the 2 min-sequestration of platelets in lungs or livers. The HoGG-induced sequestration of platelets at 2 min was blocked by high dose heparin or Cobra Venom factor. Platelet activation at 60 min was partially inhibited by dexamethasone, rhodostomin synthetic peptide 45-59, or platelet activation factor antagonist (WEB 2086). Furthermore, the thrombocytopenia could be transferred by heat (56 degrees C, 4h) treated immune sera. This suggests that HoGG-induced, non-IgE-mediated thrombocytopenia in anaphylaxis involves sequestration and activation of platelets. The sequestion in lungs occurs within 2 min and can be inhibited by high dose heparin or Cobra Venom factor. The activation of platelets involves platelet activation factor, and fibrinogen receptor.

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