Protective Humoral Immune Responses Research Articles

2 Immunological features of human immunodeficiency virus disease

Infection with the human immunodeficiency viruses results in a profound immunosuppression responsible for most of the clinical features of AIDS. The virus devastates the immune system because its main target is the T4 lymphocyte, which is the key component for generating and regulating the immune response. The cellular receptor for HIV, the membrane glycoprotein CD4, is found mainly on the surface of this major subpopulation of T lymphocytes and also on many other cell types such as those of the monocyte/macrophage series. HIV can destroy CD4 cells by direct virus cytotoxicity and indirectly through the host response against HIV-infected cells or gp120-targeted cells. Cells of the macrophage lineage are generally not destroyed but serve as a reservoir of virus. HIV also causes functional impairment in T cells, B cells and monocytes. The virus can exist in latent or chronic form. The mechanisms of cellular destruction, viral persistence and conversion to a productive infection are being studied vigorously. Host factors that may affect clinical outcome and immunological markers that may predict progression of HIV disease are presently delineated. Prolonged serological latency may follow infection with HIV. Protective humoral and cell-mediated immune responses to HIV are either poor or not sustained. Recent results on HIV-specific cytotoxic T lymphocytes are of great interest. These cytotoxic cells, particularly those directed to gp120 targets, probably contribute to cellular damage. A central question regarding immunity to HIV is its beneficial versus deleterious effects, particularly in regard to the eventual development of an AIDS vaccine.

Acquired resistance and expression of a protective humoral immune response in guinea pigs infected with Treponema pallidum Nichols.

Resistance to cutaneous syphilitic reinfection in strain 2 and strain 13 guinea pigs developed gradually 3 to 7 months after primary infection and reached maximum levels at 6 to 7 months after the induction of primary cutaneous disease. Associated with this acquired resistance was the occurrence of Arthus reactions and anamnestic-type antibody responses. Passive transfer of immune serum containing high-titered treponemal antibody into normal strain 2 guinea pigs significantly delayed the appearance and markedly diminished the severity and duration of skin lesions that developed after these recipients were challenged with treponemes but did not prevent the dissemination of organisms to the draining lymph nodes. These findings provide direct evidence that syphilitic infection elicits the formation of serum factors that are, at least, partially protective against symptomatic disease.

Host protective humoral immune responses to Schistosoma mansoni infections in the rat. Kinetics of hyperimmune serum-dependent sensitivity and elimination of schistosomes in a passive transfer system

SUMMARYA passive transfer system, dependent upon hyperimmune rat serum, was used to study in vivo protective humoral immunity to Schistosoma mansoni infection in Fischer rats. Infected recipients of hyperimmune serum exhibited a significant reduction (51%) in the number of recovered adult schistosomes relative to infected recipients of normal rat serum. Furthermore, schistosomula were equally sensitive to the effects of hyperimmune serum injected up to and including 7 days post-infection, a phenomenon which was termed ‘extended sensitivity’. Schistosomula were beginning to lose sensitivity to the effects of hyperimmune serum by the 8th day post-infection and were completely refractile by the 9th day. In addition, it was demonstrated that parasite elimination occurred after the lung stage. Some protection was also observed when hyperimmune rat serum was transferred to mice as late as 5 days post-infection.

Role of bacterial products in periodontitis: humoral immune response to Eikenella corrodens

Eikenella corrodens can induce periodontitis-like disease in gnotobiotic rats. Some components of this bacterial cell elicit measurable humoral immune response during the development of the disease, but in this system endotoxin is not among the efficient immunogens. Because no humoral immune response could be seen to the endotoxin of Eikenella corrodens it is assumed that this endotoxin can act uncontrolled in monoinfected rats. Accordingly, the lack of protective humoral immune response to pathogenic components of Eikenella corrodens may be the major factor permitting the development of the disease described here. The possibility that both cell-mediated immunity and uncontrolled endotoxic action are parts of the pathomechanism of the disease is supported by our observations.