1,721,263 research outputs found
Effetto dei virus del complesso della leucemia di Friend sullo sviluppo di cellule formanti anticorpi naturali in vitro
No full textNatura del deficit macrofagico che contribuisce allo stato immunodepressivo indotto da virus leucemogeni
No full textDifettosa interazione macrofagi-linfociti nel corso dell'infezione da virus Coxsackie B-3
No full text
Immunobiology of the Torque teno viruses and other anelloviruses
No full textMany features of the Torque teno virus and the other anelloviruses (AVs) that have been identified after this virus was discovered in 1997 remain elusive. The immunobiology of the AVs is no exception. However, evidence is progressively accumulating that at least some AVs have an interesting interplay with cells and soluble factors known to contribute to the homeostasis of innate and adaptive immunity. Evidence is also accumulating that this interplay can have a significant impact on how effectively an infected host can deal with superimposed infectious and non-infectious noxae. This review article discusses the scanty information available on these aspects and highlights the ones that would be more urgent to precisely understand in order to get an adequate assessment of how important for human health these extremely ubiquitous and pervasive viruses really are
Suppression of in vitro antibody response by spleen cells of mice infected withFriend-associated lymphatic leukemia virus
No full textThe ability of spleen cells of mice infected with oncornaviruses to depress the in vitro antibody responsiveness of normal lymphoid cells was exploited in an attempt to clarify the role played by the lymphatic leukemia virus (LLV) component in the immunodepressive properties of the Friend leukemia complex. Spleen cells of mice infected with LLV or, for comparison, with the entire complex were added to cultures of sheep erythrocyte-primed uninfected spleen cells, and the antibody-forming cells produced by the latter, after antigen restimulation, were assayed. The addition within 2 days from culture initiation of low numbers of cells infected with either virus preparation suppressed all stages of the response affecting the production of both immunoglobulin M and immunoglobulin G antibody. The activity of infected cells resisted doses of ultraviolet radiation which inhibit cell multiplication but was abolished by disrupting the cells and was prevented by the presence of anti-LLV antibodies. The LLV-infected spleen cells responsible for suppression were not removed by treatments which selectively remove or kill macrophages and exhibited surface properties of B lymphocytes. These results were interpreted as indicating that the effect is due to virus (or viral products) released by B cells. The suppressing cells in the spleens of mice in the early days of Friend leukemia complex infection presented superimposable properties, supporting the concept that their activity is also due to the LLV they release in large quantities. However, in later stages of infection, the spleens of Friend leukemia complex-infected mice also contained non-B-suppressing cells possibly derived from the proliferation of nonlymphoid LLV-producing cells caused by the neoplastic process
Reversal of a leukemia virus-induced immunodepression by macrophages in vivo and in vitro
No full text
- …
