CD8 Ratio In Blood Research Articles

Contribution of the Microbiome to Maintenance of the CD4:CD8 Ratio in Inbred and Congenic Mouse Strains

Abstract The gut microbiome is known to play an integral role in the regulation of the immune system. Previous studies indicate that species diversity and overall abundance of commensal bacteria in the gut influences immune system function by altering total T cell counts and the ratio of CD4+ to CD8+ T cells in peripheral lymphoid organs and blood. In normal individuals, the CD4:CD8 ratio is greater than one. However, the congenic B10.A mouse strain in our conventional facility consistently demonstrates an inverted CD4:CD8 ratio in a sex- and age-dependent manner, in contrast to both the parental C57Bl/10 strain and B10.A kept under SPF conditions. To determine whether this phenomenon is due to the composition and diversity of the gut microbiome affecting the homeostasis of the CD4:CD8 ratio, we altered the microbiome by supplementing the diet with the prebiotic inulin and looked for changes in the number of Peyer’s patches and changes in the CD4:CD8 ratio in gut lymphoid organs and blood in both B10.A and C57Bl/10 strains. In addition, we followed the changes in the microbiome upon treatment. We find that the mice in our facility have lower microbiome diversity and very different composition from mice kept at SPF conditions. The inulin treatment significantly increased the CD4:CD8 ratio in the blood of the C57Bl/10 mice, but not the B10.A mice. In addition, males of both strains had a significant increase in Peyer’s patch number, while the females had a significant increase in the CD4:CD8 ratio in the Peyer’s patches.

P‐9 CD8 and CD4 lymphocyte populations in blood from healthy dogs and dogs naturally infected with Ehrlichia canis

The purpose of this study was to assess the presence of an immune dysregulation in dogs naturally infected with Ehrlichia canis. We compared CD4 and CD8 lymphocyte populations in a group of dogs with ehrlichiosis and a group of healthy dogs. Thirty‐seven dogs with natural canine ehrlichiosis (Group A) and 15 unaffected dogs (Group B) were included in the study. The study of lymphocyte populations was made by flow cytometry. Monoclonal antibodies against CD3, CD4 and CD8 were used. Results obtained in this study show an inversion in the CD4:CD8 ratio in the blood of dogs with ehrlichiosis when compared with the CD4:CD8 ratio in blood from control dogs. In healthy dogs, the number of CD4 T lymphocytes was greater than CD8 T lymphocytes. However, in dogs with ehrlichiosis, the number of CD8 T lymphocytes was greater than CD4 T lymphocytes. The percentage of CD4 T lymphocytes was lower in dogs with ehrlichiosis than in healthy dogs, but significant differences were not found between both groups. However, mean value of the percentage of CD8 T lymphocytes (with respect to lymphocyte population) in dogs with ehrlichiosis (45.81 ± 20.90%) was significantly higher (P = 0.001) than in healthy dogs (25.41 ± 13.63%). These results confirm the presence of an alteration in the T lymphocyte subpopulations of dogs with ehrlichiosis, suggesting the presence of an immune dysregulation. Funding: Self‐funded.

Lymph node expansion of CD4+ lymphocytes during antiretroviral therapy.

The evolution of lymphocyte subsets was analyzed in sequential lymph nodes (LN) biopsies and compared with that in the blood of 25 human immunodeficiency virus type 1 (HIV-1)-infected patients receiving highly active antiretroviral therapy. An average of 3 biopsies were obtained from each patient, with a mean follow-up of 5.6 +/- 0.6 months. A correlation was found between the CD4:CD8 ratio in blood and in LN at baseline but not after > or = 2 months of therapy. With therapy, there was a significant increase in CD2+ cells and a much higher CD4+ cell increase and CD8+ cell decrease in LNs compared with levels in blood. A subset of patients had increased expression of Ki-67 and a decreased expression of CD8CD38 or CD3HLA-DR. Expanded CD4+ cells in LNs were mainly CD45RO+, and changes were concomitant with a decrease in LN virus load. These data demonstrate that CD4 cell reconstitution in HIV-1 infection takes place primarily in secondary lymphoid organs and is not related to a simple redistribution of cells.