THE NATURE OF THE RESPONSE OF THE CELLS OF THE SHEEP ERYTHROCYTE-TOLERANT RAT TO TRANSFERRED ALLOGENEIC LYMPHOCYTES

1972 ◽  
Vol 50 (1) ◽  
pp. 49-67 ◽  
Author(s):  
Peter McCullagh
Keyword(s):  
Sheep Erythrocyte ◽  
Allogeneic Lymphocytes

scholarly journals THE ABROGATION OF SHEEP ERYTHROCYTE TOLERANCE IN RATS BY MEANS OF THE TRANSFER OF ALLOGENEIC LYMPHOCYTES

1970 ◽  
Vol 132 (5) ◽  
pp. 916-925 ◽  
Author(s):  
Peter J. McCullagh
Keyword(s):  
Sheep Erythrocyte ◽  
Host Cells ◽  
Sheep Erythrocytes ◽  
Host Origin ◽  
Specific Reactivity ◽  
Time Required ◽  
Allogeneic Lymphocytes ◽  
In Cells

Whereas the transfer of lymphocytes from normal syngeneic donors fails to abrogate tolerance of sheep erythrocytes in rats, lymphocytes from allogeneic donors are effective. When tolerance is abrogated in this situation, the hemolysin-forming cells are predominantly of host origin. Immunological interaction between transfused lymphocytes and host cells is a prerequisite for the abrogation of tolerance. From the time required for abrogation to occur after transfer of the allogeneic cells, it is suggested that tolerance of sheep erythrocytes in rats represents the repression of a specific reactivity in cells rather than the elimination or irreversible inactivation of reactive cells. This explanation implies the existence of specifically tolerant cells.

scholarly journals MATURATION OF HEMOLYSIN-PRODUCING CELL CLONES

1970 ◽  
Vol 131 (6) ◽  
pp. 1261-1270 ◽  
Author(s):  
George C. Saunders ◽  
Douglas Swartzendruber
Keyword(s):  
Bone Marrow ◽  
Doubling Time ◽  
Sheep Erythrocyte ◽  
Mature Animal ◽  
Cell Clones ◽  
Initial Appearance ◽  
Vitro Data ◽  
In Vitro Data

Cells capable of reacting with sheep erythrocyte (SRBC) antigen to maturate and produce hemolysin appear simultaneously in the bone marrow and spleen of 1-day old Swiss-Webster mice. However, hemolysin-producing cell clones (HPCC) do not result. Complete functional precursor units generally appear in the spleens of mice older than 3 days. In vivo and in vitro data correlate well in this regard. Complete precursor units are not seen in the bone marrow and only very rarely in the thymus. The efficiency of precursor units of neonatal mice when they become functional approximates that of the mature animal when based on the doubling time of plaque-forming cells (PFC). Possible explanations of the initial appearance of incomplete precursor units have been discussed.

scholarly journals Human Articular Chondrocytes Induce Interleukin-2 Nonresponsiveness to Allogeneic Lymphocytes

Cartilage ◽  
2016 ◽  
Vol 8 (3) ◽  
pp. 300-306 ◽  
Author(s):  
Satomi Abe ◽  
Hitoshi Nochi ◽  
Hiroshi Ito
Keyword(s):  
T Cells ◽  
Articular Chondrocytes ◽  
Interleukin 2 ◽  
Flow Cytometric Analysis ◽  
Third Party ◽  
Soluble Form ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Activated T Cells ◽  
Allogeneic Lymphocytes

Introduction We previously showed that articular chondrocytes (ACs) have immune privilege and immunomodulatory functions like those of mesenchymal stem cells. To elucidate these mechanisms, we focused on interleukin-2 (IL-2), which plays critical roles in lymphocyte mitogenic activity. The purpose of this study was to explore whether ACs affect the role of IL-2 underlying immunomodulatory functions. Material and Methods Irradiated human ACs from osteoarthritis donors were used. Third-party ACs were added to the mixed lymphocyte reaction (MLR) with or without recombinant human IL-2 (rhIL-2), and the levels of IL-2 and the soluble form of the IL-2 receptor α (sIL-2Rα) protein in supernatant were measured by enzyme-linked immunosorbent assay. Recombinant human IL-2 (rhIL-2) was also added to the MLR. To detect the expression of IL-2 receptor α (CD25) on lymphocytes in the MLR, flow cytometric analysis was performed. Last, ACs and allogeneic activated CD4+ T cell were co-cultured, and the expression of CD25 on activated T cells was examined by flow cytometry. Results Third-party ACs significantly inhibited the MLR and reduced the level of sIL-2Rα in a dose-dependent manner, but did not affect the concentration of IL-2. Exogenous rhIL-2 accelerated MLR but did not rescue the inhibitory effect of ACs. ACs inhibited the expression of CD25 on activated CD4+ T cells. Discussion Our results showed that third-party ACs inhibited the proliferation of allogeneic activated lymphocytes, thereby inhibiting production sIL-2Rα, although ACs did not affect IL-2 secretion from lymphocytes. Also, ACs inhibited CD25 expression on activated CD4+ T cells. Thus, ACs inhibited the immune response of allogeneic lymphocytes by inducing IL-2 nonresponsiveness.

Immunosuppression by Murine Sarcoma Virus (Moloney)

1970 ◽  
Vol 1 (3) ◽  
pp. 288-292
Author(s):  
S. P. Chan ◽  
W. A. Hook ◽  
W. Turner ◽  
M. A. Chirigos
Keyword(s):  
Antibody Response ◽  
Survival Time ◽  
Primary Tumor ◽  
Sheep Erythrocyte ◽  
Humoral Antibody ◽  
Secondary Tumors ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Erythrocyte Antigen ◽  
Murine Sarcoma

Infection of mice with the murine sarcoma virus (Moloney) markedly suppressed the humoral antibody response to sheep erythrocyte antigen injected 10 days after infection, when tumor size was maximal, and on day 26, when primary tumors had partially regressed. Humoral antibody response was also inhibited when antigen was injected at the time secondary tumors and metastases were evident. No significant suppression of humoral antibody was seen when mice were injected with sheep erythrocyte antigen 5 days after virus infection. Inhibition of the cellular immune response of murine sarcoma virus (Moloney)-infected mice, as measured by the increased survival time of skin grafts, was also determined. Mice that were infected 5 days prior to grafting demonstrated prolonged survival of grafts, suggesting a suppression of cellular immunity. These mice had a graft survival time 14 days greater than noninfected controls. No significant prolongation of graft survival was seen in mice grafted at the times of maximum primary tumor growth, of primary tumor regression, or when secondary tumors had appeared.

Role of protein kinases in regulating sheep erythrocyte K-Cl cotransport

1996 ◽  
Vol 271 (1) ◽  
pp. C255-C263 ◽  
Author(s):  
P. W. Flatman ◽  
N. C. Adragna ◽  
P. K. Lauf
Keyword(s):  
Protein Kinases ◽  
Tyrosine Kinases ◽  
Kinase Inhibitor ◽  
Sheep Erythrocyte ◽  
Inhibition Constant ◽  
Calyculin A ◽  
Sheep Erythrocytes ◽  
A 23187 ◽  
Maximal Activation

K-Cl cotransport in sheep erythrocytes can be activated by treatment either with A-23187 and EDTA to reduce concentration of internal ionized Mg [Mg]i) to submicromolar levels, with staurosporine, a potent kinase inhibitor, or with N-ethylmaleimide (NEM). Activation by these maneuvers is prevented and reversed by genistein [inhibition constant (Ki) of 15 microM], which inhibits tyrosine kinases (TK). The related glycosidated compound genistin, which does not inhibit TK, does not inhibit transport, whereas another TK inhibitor, tyrphostin B46, inhibits both basal and stimulated transport (Ki of 28 microM). Cotransport activation by NEM is prevented and reversed by the phosphatase inhibitor, calyculin A, and activation by staurosporine occurs only if cells contain ATP. Increasing [Mg]i inhibits cotransport in the presence of calyculin A whether or not staurosporine is present as well. Our work suggests that genistein inhibits cotransport through a TK and that staurosporine and NEM activate cotransport, probably through inhibition of other kinases, causing stimulation through dephosphorylation of a protein (possibly the transporter itself) be a serine/threonine phosphatase. [Mg]i inhibits cotransport by activating a kinase (concentration for half-maximal activation of 10 microM) that phosphorylates this protein.

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