Compared with at admission, at discharge the MP patients had significantly increased levels of lymphocyte differential (44.3% vs. 28.8%, respectively; p = 0.001), total IgG (921 vs. 893 mg/dL, respectively; p = 0.01) and platelet count (371,000/μL vs. 262,000/μL, respectively; p < 0.001) (data not shown).
Increased levels of lymphocyte-activation antigens, including CD98, have been found at the cell surface of intestinal B cells, CD4+ T cells and CD8+ T cells isolated from patients with inflammatory bowel disease [41].
In both tumor types, a significant decrease in the percentages of cells that were CD31+, as a marker of ECs was detected (Fig. 2e) and this was associated with significantly increased levels of CD8+ lymphocytes in the TDG-treated B16F10 and 4T1 tumors (Fig. 2f).
Biological studies have demonstrated increased levels of CD3+/CD25+ lymphocytes [ 5], HTLV-I proviral load and HTLV-I tax/rex mRNA expression [ 6, 7], HTLV-I specific IgA [ 8], soluble interleukin-2 receptors [ 9], beta-chemokines [ 7] and soluble intracellular adhesion molecule-1 (ICAM-1) [ 10], in bronchoalveolar lavage fluid from HTLV-I infected humans.
Increased levels of all the lymphocyte subsets have been found and some authors have reported a fall in the CD4/CD8 ratio [ 6].
It appears that B cells are undergoing proliferation and isotype switching as increased levels of IgG-bearing lymphocytes have been found in the mucosal lesion of ulcerative colitis [ 9].
Male mice have increased levels of TLR4 protein on splenic lymphocyte populations compared to females.
Intestinal bacterial overgrowth and translocation, both common in cirrhosis with ascites, may lead to the activation of monocytes and lymphocytes, increased levels of proinflammatory cytokines, and enhanced synthesis of nitric oxide present in cirrhosis.
Forsberg et al. [ 39] previously reported similar findings, showing increased levels of IL-10 in intraepithelial lymphocytes in the context of celiac disease.
Moreover, increased levels of CCR5 molecules on CD3+ lymphocytes were also observed in AVL/HIV-AIDS [ 20], suggesting that Leishmania infection could favor HIV-1 entry into its target cells through this receptor.
Consistently, we found that when WBCs were treated with metHb, the neutrophils and monocytes within the WBC population produced increased levels of ROS as compared to lymphocytes (Fig. 3d).
