Abstract
The genetic control of eosinophilia has been studied in congenic strains of mice. Eosinophilia was induced with cyclophosphamide followed by keyhole limpet hemocyanin in complete Freund's adjuvant. After this treatment, BALB/c mice developed a high eosinophil response, whereas CBA, C57BL and A/J mice developed a low one. The major histocompatibility complex (MHC) was found to exert a control on eosinophilia, as B10.D2 mice developed a higher eosinophil response than B10, B10.A, or B10.BR. BALB/c-H-2k mice had a lower response than BALB/c, and A.TL mice had a higher response than A/J or A.TH. If a single gene within the MHC is responsible for these effects, the most likely position for it is in the vicinity of the Tla locus. Splenectomy reduced eosinophilia in BALB/c and A.TL mice, but not in A/J mice, indicating that the spleen is a significant site of eosinophil production in high responder strains.
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