Humoral and cellular immunity in spontaneous feline infectious peritonitis

HUMORAL AND CELLULAR IMMUNITY IN SPONTANEOUS FELINE INFECTIOUS PERITONITIS Paltrinieri S.*, Cammarata Parodi M.**, Cammarata G.**, Comazzi S.* * Istituto di Patologia Generale Veterinaria - Milano - Italy; ** Istituto di Anatomia Patologica Veterinaria e Patologia Aviare - Milano - Italy Vascular lesions in Feline Infectious Peritonitis (FIP) are thought to be caused by a type III hypersenstivty reaction, while histology of the granulomas suggest a type IV hypersensitivity. To further investigate the pathogenesis of the disease we analized some aspects of humoral and cellular immunity in FIP. Haematology, antibody titers and protein electrophoresis in serum and in effusions from 48 FIP affected cats were studied. The results were compared with those of 20 healthy cats. The distribution of the immune cell and of the virus in FIP lesions were also studied by immunohistochemistry using antibodes against myelomonocytic (MAC387), and lymphoid (CD3, CD4 and CD8 for T-cells and IgM and IgG for B-cells) antigens. Seropositive animals (antibody titer>1:100) were present either among the FIP infected cats (73%) either among the healthy cats (72%). FIP infected cats had neutrophilic leukocytosis (P>0.05), lymphopenia (P<0.05) and hyperglobulinemia (P<0.01) with increased 2 (P<0.05) and  globulins (P<0.001). Hypergammaglobulinemia was not related to the antibody titers, suggesting the presence of other proteins with  motility (e.g. complement fractions such as C1q). These changes were found either in effusive or in non effusive FIP. The electrophoretic pattern of the effusions was always similar to those of the corresponding serum. Antibody titers higher than those of the corresponding serum were often detected in the effusions. Immunohistochemical findings were not related to the antibody titers, but they were related to the histology of the lesions. In cellular foci of FIP lesions many virus-infected macrophages and few lymphocytes, mainly CD4+ve, were found. Extracellular viral and myelomonocytic antigen were also detectable in the foci with intercellular necrosis. Only few FIPV-infected cells were present at the periphery of the larger necrotic foci: in these lesions MAC387+ve cells were mainly neutrophils, with many MAC387-ve macrophages, may be due to their activated state: a mild number of lymphocytes, with an increasing percentage of CD8+ve cells were present. Lymphocytes were more abundant when cellular foci and FIP infected macrophages were centered around neoformed vessels. IgM and IgG exposing B-cells were always few and scattered. In conclusion the simoultaneous analysis of body fluids and of the cellular composition of the lesions showed a complex immune status, on which type III and type IV hypersenstivty could cohexist.