scholarly journals Interleukin 2 induces a rapid increase in intracellular pH through activation of a Na+/H+ antiport. Cytoplasmic alkalinization is not required for lymphocyte proliferation.

1985 ◽  
Vol 260 (23) ◽  
pp. 12500-12507 ◽  
Author(s):  
G B Mills ◽  
E J Cragoe ◽  
E W Gelfand ◽  
S Grinstein
Keyword(s):  
Intracellular Ph ◽  
Lymphocyte Proliferation ◽  
Interleukin 2

scholarly journals Regulation of interleukin 2-driven T-lymphocyte proliferation by prolactin.

1990 ◽  
Vol 87 (16) ◽  
pp. 6460-6464 ◽  
Author(s):  
C. V. Clevenger ◽  
D. H. Russell ◽  
P. M. Appasamy ◽  
M. B. Prystowsky
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Interleukin 2 ◽  
T Lymphocyte Proliferation

scholarly journals Immunologic correlates of spontaneous lymphocyte proliferation in human T-lymphotropic virus infection

Blood ◽  
1991 ◽  
Vol 78 (1) ◽  
pp. 169-174 ◽  
Author(s):  
HE Prince ◽  
H Lee ◽  
ER Jensen ◽  
P Swanson ◽  
D Weber ◽  
...  
Keyword(s):  
Lymphocyte Proliferation ◽  
Mononuclear Cells ◽  
Interleukin 2 ◽  
Serum Levels ◽  
Control Group ◽  
Relative Distribution ◽  
T Lymphotropic Virus ◽  
Soluble Cd25 ◽  
Spontaneous Proliferation ◽  
Antibody Levels

Abstract Previously we showed that mononuclear cells from about half of human T- lymphotropic virus (HTLV)-seropositive persons exhibit spontaneous proliferation in vitro. We sought to determine if proliferation was associated with other immunologic changes characteristic of HTLV infection. The parameters assessed were (1) percentages of lymphocytes expressing CD4 and/or CD25 (interleukin-2 receptor), (2) serum levels of soluble CD25, (3) serostatus for other viruses, (4) anti-HTLV antibody levels, and (5) HTLV type determined by polymerase chain reaction or serologic reactivity with type-specific peptides. The proliferation+ HTLV (PROL+) group, proliferation HTLV (PROL-) group, and control group showed similar percentages of CD4+, CD25+, and CD4+CD25+ lymphocytes; serum levels of soluble CD25 were also similar. Antibodies to cytomegalovirus, hepatitis B core, and hepatitis C were present in similar proportions of PROL+ and PROL+ groups. However, a significant association was found between spontaneous proliferation and anti-HTLV antibody levels; sera from 67% of PROL+ persons, but only 18% of PROL- persons, required dilution to yield absorbance values within the linear range of the anti-HTLV antibody assay. In the PROL+ group, persons whose sera required the most dilution had proliferative responses significantly higher than those whose sera required no dilution. The PROL+ and PROL groups were similar with regard to the relative distribution of HTLV-I and HTLV-II infection. These findings indicate that HTLV-related spontaneous lymphocyte proliferation is related to levels of circulating anti-HTLV antibodies, and characterizes both HTLV-I and HTLV-II infection.

Influence of exercise on the immune function of rats of various ages

1988 ◽  
Vol 64 (5) ◽  
pp. 1997-2001 ◽  
Author(s):  
M. A. Pahlavani ◽  
T. H. Cheung ◽  
J. A. Chesky ◽  
A. Richardson
Keyword(s):  
Immune Function ◽  
Concanavalin A ◽  
Lymphocyte Proliferation ◽  
Interleukin 2 ◽  
Training Period ◽  
Sedentary Control ◽  
Age Related ◽  
Old Rats ◽  
Spleen Lymphocytes ◽  
F344 Rats

The purpose of this study was to determine whether exercise could prevent the age-related decline in mitogenesis, which has been well documented in rats, mice, and humans. At 1, 6, 12, and 18 mo of age, male Fischer F344 rats were subjected daily to swimming exercise for 6 mo. At the end of the 6-mo training period, spleen lymphocytes were isolated from the exercised rats and from age-matched sedentary controls. The induction of lymphocyte proliferation was measured with the mitogens concanavalin A (ConA) and lipopolysaccharide (LPS). In addition, the ability of the lymphocytes to produce interleukin 2 (IL 2) in response to ConA induction was measured. ConA- and LPS-induced proliferation decreased 41–63% between 7 and 25 mo of age in both exercised and sedentary control rats. ConA-induced IL 2 production decreased 42 and 62% between 7 and 25 mo of age for exercised and sedentary control rats, respectively. Although the age-related decline in mitogen-induced proliferation and IL 2 production was smaller in exercised rats, this was due to a lower level of mitogenesis and IL 2 production in lymphocytes from young exercised rats. Exercise resulted in a significant decrease (23–32%) in mitogen-induced lymphocyte proliferation and IL-2 production in 7-mo-old exercised rats compared with 7-mo-old sedentary rats. However, in the 18- and 24-mo-old rats, mitogen-induced lymphocyte proliferation and IL 2 production was not significantly different between exercised and sedentary control rats.

scholarly journals Inhibition of prostaglandin E2 restores defective lymphocyte proliferation and cell-mediated lympholysis in recipients after allogeneic marrow grafting

Blood ◽  
1986 ◽  
Vol 68 (1) ◽  
pp. 102-107 ◽  
Author(s):  
HG Klingemann ◽  
MS Tsoi ◽  
R Storb
Keyword(s):  
Prostaglandin E2 ◽  
Lymphocyte Proliferation ◽  
Chronic Gvhd ◽  
Interleukin 2 ◽  
In Vitro Tests ◽  
Lymphocyte Function ◽  
T Lymphocyte Proliferation ◽  
Long Term Survivors

Abstract Prostaglandins are said to influence T and B cell function by inhibiting the generation of interleukin 2 (IL 2) and the formation of suppressor lymphocytes. After bone marrow transplantation, patients usually have a profound immunodeficiency that persists in recipients with chronic graft-v-host disease (GVHD) and generally resolves in long- term survivors without GVHD. In vitro tests of lymphocyte function such as allogeneic mixed lymphocyte culture (MLC) and cell-mediated lympholysis (CML) have been shown to be impaired in many patients. We postulated that prostaglandin E2 (PGE2) plays a role in the impaired in vitro tests. To test this hypothesis, we studied in vitro tests in the presence of PGE2 antagonists, indomethacin, and anti-PGE2 antiserum with cells from 22 short-term patients (less than 100 days postgrafting) and 32 long-term survivors with or without GVHD. Results show that blockade of PGE2 release by indomethacin and anti-PGE2 significantly (P less than .01) enhanced the MLC (+67%) and the CML responses (+10.5%) of cells from long-term survivors with chronic GVHD but not from those of long-term, stable recipients. No enhancement of MLC and CML activity was observed with cells from donors of long-term recipients. In patients shortly after marrow grafting, enhancement in the MLC was not significant. However, CML activity in this patient group was significantly increased (+12.5% in recipients with no GVHD, 8.5% in those with acute GVHD, P less than .01). Indomethacin also suppressed the activity of nonspecific suppressor cells in patients with chronic GVHD. When cells from patients with chronic GVHD were treated with recombinant IL 2 and IL 2 combined with indomethacin, it was possible to get an additional augmentation of lymphocyte proliferation after the addition of indomethacin to IL 2-treated cultures. Thus it is very likely that PGE2 inhibits T lymphocyte proliferation, not exclusively by inhibition of IL2 production or activity. We conclude that PGE2, among other factors, may play a role in the pathogenesis of the immunodeficiency after transplantation. PGE2 does not act primarily by interfering with IL2 but presumably by inducing a suppressorlike activity.

Human lymphocyte proliferation. Relationships between cell cycle events and interleukin 2 (IL-2) production

1982 ◽  
Vol 70 (2) ◽  
pp. 382
Author(s):  
F. Kristensen ◽  
F. Bettens ◽  
C. Walker ◽  
F. Joncourt ◽  
A.L. de Weck
Keyword(s):  
Cell Cycle ◽  
Human Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Interleukin 2

Selenium and Immune Cell Functions. I. Effect on Lymphocyte Proliferation and Production of Interleukin 1 and Interleukin 2

1990 ◽  
Vol 193 (2) ◽  
pp. 136-142 ◽  
Author(s):  
L. Kiremidjian-Schumacher ◽  
M. Roy ◽  
H. I. Wishe ◽  
M. W. Cohen ◽  
G. Stotzky
Keyword(s):  
Lymphocyte Proliferation ◽  
Immune Cell ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Cell Functions

scholarly journals Kinesin Motor Domain of Leishmania donovani as a Future Vaccine Candidate

2008 ◽  
Vol 15 (5) ◽  
pp. 836-842 ◽  
Author(s):  
Ayan Dey ◽  
Pawan Sharma ◽  
Naresh Singh Redhu ◽  
Sarman Singh
Keyword(s):  
Visceral Leishmaniasis ◽  
Lymphocyte Proliferation ◽  
Leishmania Donovani ◽  
Mononuclear Cells ◽  
Vaccine Candidate ◽  
Ex Vivo ◽  
Interleukin 2 ◽  
Motor Domain ◽  
Enzyme Linked Immunosorbent Assay ◽  
Kinesin Motor

ABSTRACT Visceral leishmaniasis (VL) is one of the important parasitic diseases, with approximately 350 million people at risk. Due to the nonavailability of an ideal drug, development of a safe, effective, and affordable vaccine could be a solution for control and prevention of this disease. The present study was carried out to examine the immunological potential of kinesin protein from the microtubule locus of Leishmania donovani as a suitable vaccine candidate. In silico analysis of this region revealed clusters of major histocompatibility complex class I and II binding epitopes in its motor domain region. A recombinant protein was expressed from this region and named rLvacc. The antigenicity and immunogenicity studies of this protein by Western blot analysis revealed that rLvacc is strongly recognized by sera from acute VL patients. To evaluate its immunogenicity, peripheral blood mononuclear cells from cured VL patients were separated, and a lymphocyte proliferation assay was carried out in the presence of rLvacc. After lymphocyte proliferation, the pooled culture supernatant was assayed for anti-rLvacc antibody titers using an enzyme-linked immunosorbent assay. The results showed that immunoglobulin G2 (IgG2) subtype antibodies were predominant, while IgG1 subtype antibodies were produced in very low titers. On the basis of these ex vivo preliminary findings, its immunogenicity was studied in BALB/c mice. Vaccination with the DNA construct generated a good cellular immune response with significant increases in gamma interferon and interleukin-2 (IL-2) cytokine levels (Th1), but no increase in IL-4 levels (Th2). Taken together, our findings suggest the kinesin motor domain region of L. donovani as a potential vaccine candidate against visceral leishmaniasis.

scholarly journals Unsaturated fatty acids suppress interleukin-2 production and transferrin receptor expression by concanavalin A-stimulated rat Iymphocytes

1992 ◽  
Vol 1 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Philip C. Calder ◽  
Eric A. Newsholme
Keyword(s):  
Fatty Acids ◽  
Transferrin Receptor ◽  
Lymphocyte Proliferation ◽  
Culture Medium ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
T Lymphocyte Proliferation ◽  
Transferrin Receptor Expression

The proliferation of T-lymphocytes is dependent upon their ability to synthesize and secrete the cytokine, interleukin-2, and to express cell surface receptors for interleukin-2 and transferrin. We have previously reported that certain fatty acids inhibit mitogen-stimulated T-lymphocyte proliferation. We now report that unsaturated fatty acids decrease the concentration of interleukin-2 in the culture medium of such cells by up to 45%. This suggests that unsaturated fatty acids inhibit lymphocyte proliferation by suppressing interleukin-2 production. However, lymphocyte proliferation was only partially restored by addition of exogenous interleukin-2 to cell culture medium in the presence of unsaturated fatty acids, indicating that these fatty acids also affect other processes involved in the control of proliferation. Saturated fatty acids, which also inhibit lymphocyte proliferation, did not affect the interleukin-2 concentration in the culture medium suggesting a different mechanism for their action. Neither saturated nor unsaturated fatty acids affected the expression of the interleukin-2 receptor by mitogenstimulated lymphocytes. In contrast, unsaturated fatty acids decreased expression of the transferrin receptor by up to 50%. These observations suggest that the mechanism by which unsaturated fatty acids inhibit lymphocyte proliferation involves suppression of interleukin-2 production and of transferrin receptor expression. The mechanism for the inhibitory action of saturated fatty acids is not clear.

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