T‐cell‐receptor dose and the time of treatment during murine retrovirus infection for maintenance of immune function

Abstract

SUMMARYC57BL/6 mice were injected with different doses of human T-cell receptor (TCR) Vb8.1 CDR1 peptide at different times after murine retrovirus (LP-BM5) infection. Injection with TCR Vb8.1 CDR1 peptide largely prevented the retrovirus-induced reduction in B-and T-cell proliferation, and T-helper 1 (Th1) cytokines [interleukin-2 (IL-2) and interferon-g (IFN-g)] secretion. It also suppressed T-helper 2 (Th2) cytokines (IL-6 and IL-10) production, which was stimulated by retrovirus infection. These effects were accomplished using at least 100 m g of peptide per mouse and the most effective dose of peptide had to be given within 4 weeks after retrovirus infection. Immunization with doses above 100 m g/mouse as long as 4 weeks postinfection maintained natural killer (NK) cell activity during retrovirus infection. Reducing the dose of peptide or delaying it until the disease progressed towards early murine acquired immune deficiency syndrome (AIDS) allowed development of immune dysfunction. These studies provide data suggesting that immune dysfunction, induced by murine retrovirus infection, was largely prevented by TCR Vb CDR1 peptide injection.

Prevention of immune dysfunction and vitamin E loss by dehydroepiandrosterone and melatonin supplementation during murine retrovirus infection

“…LP‐BM5 retrovirus was administered i.p. to mice in 0·1 ml with an esotropic titer (XC) of 4·5 log 10 plaque‐forming units (PFU)/ml, which induces disease with a time course comparable to that previously published 16 . Uninfected mice were injected with complete culture medium [CM, RPMI‐1640 containing 10% fetal calf serum (FCS), 2 mm glutamine, 100 U/ml penicillin and streptomycin] as controls.…”

Vitamin E–loaded dialyzer resets PBMC-operated cytokine network in dialysis patients

“…We have described [3] a novel aspect of the immune dysfunction associated with RDT [i.e., an imbalanced activity of the two T helper (Th) lymphocyte subsets], which results in an overwhelming prevalence of Th2 over Th1 cells. This imbalance leads to high constitutive production of interleukin (IL)-4 and IL-10, and suppression of interferon-c (IFN-c) (i.e., a configuration of cytokine network that may play a pivotal role in causing immunodeficiency) [4][5][6][7].…”

Comparative Proteomic Analysis of Peritoneal Dialysate from Chronic Glomerulonephritis Patients

“…However, the inactivation of its function by oxidants resulted in proteolytic injury and unrestrained synthesis of inflammatory mediators during peritonitis [22]. Histidine-rich glycoprotein (P07/P08) has been shown to bind heparin [23], plasminogen [24], and fibrinogen [25] and to regulate aspects of the immune system [26, 27]. Histidine-rich glycoprotein is an important regulator of immune complexes uptake by monocytes [28].…”