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Departments of
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Medicine,
Pediatrics,
Pathology, and
§
Molecular and Human Genetics,
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Howard Hughes Medical Institute, and
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Department of Microbiology and Immunology, Baylor College of Medicine, Houston, TX 77030
A murine model of IgA deficiency has been established by targeted
deletion of the IgA switch and constant regions in embryonic stem
cells. B cells from IgA-deficient mice were incapable of producing IgA
in vitro in response to TGF-ß. IgA-deficient mice expressed higher
levels of IgM and IgG in serum and gastrointestinal secretions and
decreased levels of IgE in serum and pulmonary secretions. Expression
of IgG subclasses was complex, with the most consistent finding being
an increase in IgG2b and a decrease in IgG3 in serum and secretions. No
detectable IgA Abs were observed following mucosal immunization against
influenza; however, compared with those in wild-type mice, increased
levels of IgM Abs were seen in both serum and secretions. Development
of lymphoid tissues as well as T and B lymphocyte function appeared
normal otherwise. Peyer’s patches in IgA-deficient mice were well
developed with prominent germinal centers despite the absence of IgA in
these germinal centers or intestinal lamina propria. Lymphocytes from
IgA-deficient mice responded to T and B cell mitogens comparable to
those of wild-type mice, while T cells from IgA-deficient mice produced
comparable levels of IFN-
and IL-4 mRNA and protein. In conclusion,
mice with targeted deletion of the IgA switch and constant regions are
completely deficient in IgA and exhibit altered expression of other Ig
isotypes, notably IgM, IgG2b, IgG3, and IgE, but otherwise have normal
lymphocyte development, proliferative responses, and cytokine
production.
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