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Rabbit anti-mouse mu-chain serum was used to deplete specifically IgM-bearing B cells and B cell function in BALB/c mice. B cell-depleted and normal littermates were infected via the cornea with herpes simplex virus type 1 (HSV-1) at 4 to 5 wk of age. B cell-depleted mice had a reduced number of lymphocytes bearing surface immunoglobulin and a greatly reduced ability to produce antibody. Mortality was reduced from 89% in normal controls to 42% in B cell-depleted mice (p less than 0.001) and peak virus shedding from eyes was also reduced as much as 90% in the B cell-depleted mice (p less than or equal to 0.0005). These results support the hypothesis that a B cell function of normal mice somehow contributes directly or indirectly to the enhanced mortality of mice infected with HSV.

Although the association between HLA‐B27 and ankylosing spondylitis (AS) is well established, the mechanism governing this association remains unknown. Although ∼90% of affected individuals possess the HLA‐B27 antigen, HLA‐B27 is also present in ∼8% of the normal population. This article examines the association by reviewing recent literature. Theories proposed have ranged from HLA‐B27's possible role as a marker for an AS susceptibility gene to the possibility of HLA‐B27 being a direct contributor to disease. Theories suggest the presence of pathogenic and benign forms of the antigen, as well as interaction with genetic and environmental factors in disease development. Recent investigations have focused on a link with Klebsiella and its role in a “cross‐reactive” mechanism with HLA‐B27 in AS development. Studies to date have not provided conclusive evidence on the exact mechanism by which HLA‐B27 predisposes individuals to the development of disease. The importance of isolating a specific causative agent for AS is discussed.

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