Dynamics of B-lymphocytes in the lungs of mice exposed to aerosolized influenza virus

Abstract

Immunoglobulin-containing cells were revealed by immunofluorescence in lung sections from mice infected with influenza virus by the aerosol route. The numbers of immunoglobulin A (IgA)and IgM-containing cells were increasing by day 3 of the infection, whereas IgG-containing cells appeared a few days later. The responding B-cell populations appeared in two principal locations: along major airways and in consolidated lesions within lung parenchyma. IgA-containing cells were the most numerous isotype, occurring predominantly in the lamina propria of the airways. IgG-containing cells were the least frequently encountered class along airways and appeared most often within consolidated lung lesions in clustered groupings. Cells staining for mu chain appeared along the airways and in lung lesions. The population of IgM-containing cells declined approximately 30 days after infection. Cells producing alpha and gamma chains were still numerous on day 46. Assays for virus-reactive antibodies in lung secretions were positive on day 8 of the infection. The IgM titers were the first to decline, but virus-binding antibodies for all classes were still present on day 33. The implications of immune responses in viral pneumonitis were considered.

Local and peripheral cell‐mediated immune response to influenza virus in mice

“…After VA administration, a change in cell population distribution was found. Changes in cell population were also noted by others following IN administration of influenza [Owens et al, 1981;Scott and Walker, 1976;Wyde and Cate, 19781. The CMI response following IN application preceded local or humoral antibody response in the case of VA, as found by others [Wells et al, 19791, and was also induced by VF preparation; nevertheless, VF failed to induce local antibody response against the two surface glycoproteins, hemagglutinin and neuraminidase. Lack of local secretory antibodies following local application of VF was corroborated by the failure of such preparations to induce augmentation in the number of B surface IgAbearing lymphocytes, in contrast to the increased percentage of this cell type following immunization with VA.…”

Immunocytochemical identification and quantitation of the mononuclear cells in the cerebrospinal fluid, meninges, and brain during acute viral meningoencephalitis.

“…B cells comprise only a very small proportion of the mononuclear cells early in the viral inflammatory process, but, like macrophages, increase in later phases. B cells have been shown to appear late in the inflammatory response to poliomyelitis in humans (36), influenza pneumonia in mice (37), and the autoimmune demyelinating disease, experimental allergic encephalomyelitis (38,39). It is likely that B cells, like monocytes, also enter local inflammatory reactions in response to lymphokines produced by T cells of the Lyt-1 phenotype already present at the site of antigenic stimulation in the CNS (34).…”

Role of the B‐cell response in recovery of mice from primary influenza virus infection

“…It is relatively small when measured as free antibody in serum but substantial when measured as ASC response in draining lymph nodes (28). Finally, although the therapeutic activities of mAb were determined by treatment of mice 1 day after infection (to reduce the likelihood of outgrowth of viral escape mutants), extensive pulmonary infections can be cured with polyspecific mixtures of iTiAh (48), Interestingly, delayed treatment does not require much larger antibody doses than early treatment, prestmiably because u-ansudation is greatly increased by the inflammatory process at this stage (56).…”