Suppressor activity of spleen cells in drug-induced immunologic tolerance

1978 ◽  
Vol 86 (5) ◽  
pp. 1469-1473
Author(s):  
V. M. Pisarev ◽  
A. Yu. Volgin
Keyword(s):  
Immunologic Tolerance ◽  
Spleen Cells ◽  
Drug Induced ◽  
Suppressor Activity

scholarly journals IMMUNOPATHOGENESIS OF ACUTE CENTRAL NERVOUS SYSTEM DISEASE PRODUCED BY LYMPHOCYTIC CHORIOMENINGITIS VIRUS

1972 ◽  
Vol 135 (4) ◽  
pp. 874-889 ◽  
Author(s):  
Donald H. Gilden ◽  
Gerald A. Cole ◽  
Neal Nathanson
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Antigen ◽  
Central Nervous System Disease ◽  
Lymphocytic Choriomeningitis ◽  
Lymphoid Cells ◽  
Intracerebral Injection ◽  
Spleen Cells ◽  
Drug Induced ◽  
Immune Spleen Cells

Lymphocytic choriomeningitis (LCM) virus carriers were established by intracerebral inoculation of adult BALB/c mice followed by a single dose of cyclophosphamide (CY) (150 mg/kg) 3 days after infection, and by intracerebral injection within 24 hr of birth. These carriers were then adoptively immunized with spleen cells or serum from immune or normal BALB/c donors. Transfer of immune spleen cells into drug-induced carriers consistently resulted in acutely fatal choriomeningitis, histologically strikingly similar to classical LCM. Normal spleen cells or immune serum failed to produce either central nervous system (CNS) pathology or illness with any regularity. In addition, focal necrosis of the cerebellum was seen after adoptive immunization of drug-induced carriers but only when mice received cells at least 3 wk after inoculation, which is probably explained by the gradual spread of infection from membranes to the neural parenchyma during the first month after establishment of the carrier state in adult mice. Immune spleen cells, when transferred to neonatal carriers, led to a decrease in virus titers in blood and brains and to development of antibody without acute CNS disease. It appears that the production of fatal choriomeningitis after LCM infection is determined in part by the distribution of viral antigen, and this is markedly different in neonatal and drug-induced carriers at the time of cell transfer. Another factor of potential importance is the much higher level of circulating viral antigen in the plasma of neonatal than in that of drug-induced LCM carriers. Classical LCM disease can only be transferred by immune lymphoid cells and not by antiserum. Furthermore, little or no complement-fixing (CF) antibody was found in the plasma of mice dying of acute choroiditis. These observations strongly suggest that acute choroiditis is dependent upon the cell-mediated immune response.

Suppressor Activity in the Supernatant of T Cell Clones Derived from Chimeric Mouse Spleen Cells

Immunobiology ◽  
1988 ◽  
Vol 177 (1) ◽  
pp. 91-103
Author(s):  
Masahiro Imamura ◽  
Hisao Fujimoto ◽  
Takashi Fukuhara ◽  
Masanobu Kobayashi ◽  
Satoshi Hashino ◽  
...  
Keyword(s):  
T Cell ◽  
Mouse Spleen ◽  
Chimeric Mouse ◽  
Spleen Cells ◽  
Suppressor Activity ◽  
T Cell Clones ◽  
Cell Clones

scholarly journals A natural model of immunologic tolerance. Tolerance to murine C5 is mediated by T cells, and antigen is required to maintain unresponsiveness.

1982 ◽  
Vol 156 (2) ◽  
pp. 567-584 ◽  
Author(s):  
D E Harris ◽  
L Cairns ◽  
F S Rosen ◽  
Y Borel
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Lymphoid Cells ◽  
Immunologic Tolerance ◽  
Secondary Response ◽  
Spleen Cells ◽  
Physiological Concentration ◽  
Significant Drop ◽  
Natural Form

A unique experimental model is described, where natural immunologic tolerance to a well-defined soluble native antigen (murine C5) is examined in congenic strains of mice that differ only by the presence or the absence of C5. A highly sensitive hemolytic assay was developed to detect nanogram amounts of C5 as well as an assay of anti-C5 inhibition of C5 hemolytic activity. The latter was more sensitive than immunodiffusion. Two reciprocal approaches were used to study the cellular basis of tolerance in irradiated hosts of either strain. In the first, lymphoid cells from either strain were transferred to irradiated B10.D2OSN hosts that were lacking C5 and so would not hinder detection of anti-C5 antibody upon challenge with murine C5. Second, lymphoid cells from either strain were transferred to irradiated B10.D2NSN hosts, whose native C5 provided the antigenic stimulus. The immune response of whole nonadherent spleen cell suspension as well as mixtures of T and B cells (separated on the basis of surface immunoglobulin) from either strain were studied. In addition, the duration of tolerance and the antigen requirement to maintain it in irradiated C5-deficient hosts repopulated with C5-sufficient spleen cells was examined. The positive control of irradiated C5-deficient hosts repopulated with syngeneic spleen cells showed a primary and secondary response to immunization. In contrast, C5-sufficient spleen cells failed to respond both in the primary and the secondary response. Because the unresponsiveness was not caused by antigen carryover and was not antigen specific, it represents central tolerance. In C5-sufficient irradiated hosts (where immunization was not required and antigen was present in natural form and physiological concentration), transfer of C5-deficient cells mediated a drop in C5 levels to 10-20% of that noted in unreconstituted controls. T and B cell mixing experiments from the two strains into deficient or sufficient hosts demonstrated that tolerance is T cell dependent and that C5-sufficient or -deficient B cells could cooperate with nontolerant C5-sufficient T cells to produce significant anti-C5 antibody or mediate a significant drop in C5 levels. In addition, the presence of antigen was necessary to maintain tolerance. In conclusion, these results show that (a) natural tolerance to C5 is an active process that is T cell dependent and requires the presence of antigen; (b) in this natural model, clonal abortion does not seem to occur; and (c) both tolerant and nontolerant B cells retain the capacity to produce autoantibody.

The effect of allogeneic spleen cells on the induction of immunologic tolerance

1974 ◽  
Vol 14 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Janice Lankford ◽  
Rebecca Blackstock ◽  
Victoria Szatalowicz ◽  
Richard M. Hyde
Keyword(s):  
Immunologic Tolerance ◽  
Spleen Cells

scholarly journals STUDIES ON THE MECHANISM OF PENICILLIN-INDUCED FEVER

1972 ◽  
Vol 136 (2) ◽  
pp. 227-240 ◽  
Author(s):  
Michael J. Chusid ◽  
Elisha Atkins
Keyword(s):  
Serum Protein ◽  
The Other ◽  
Endogenous Pyrogen ◽  
Spleen Cells ◽  
Drug Induced ◽  
Blood Leukocytes ◽  
Protein Conjugate ◽  
Other Hand

Rabbits immunized to benzylpenicillin G responded with fever when challenged with a penicillin-serum protein conjugate, but not with penicillin itself. After one or two challenges with conjugate, the rabbits became unresponsive (tolerant) to further injections. This form of hypersensitivity was transferable with plasma of immunized donors to normal rabbits. Blood leukocytes of immunized rabbits incubated with penicillin-protein conjugate and hypersensitive serum released endogenous pyrogen in vitro. Spleen cells from the same animals, on the other hand, were inactive when incubated with this antigen in vitro. These experiments appear to be the first to demonstrate in vitro a possible mechanism of drug-induced fever.

scholarly journals Regulatory mechanisms in cell-mediated immune responses. IV. Expression of a receptor for mixed lymphocyte reaction suppressor factor on activated T lymphocytes.

1976 ◽  
Vol 144 (5) ◽  
pp. 1214-1226 ◽  
Author(s):  
S S Rich ◽  
R R Rich
Keyword(s):  
T Lymphocytes ◽  
Mixed Lymphocyte Reaction ◽  
Suppressor Cell ◽  
Lymphoid Cells ◽  
Resting Cells ◽  
Spleen Cells ◽  
Con A ◽  
Suppressor Activity ◽  
Suppressor Factor ◽  
Genetic Homology

Suppression of the mixed lymphocyte reaction (MLR) by a soluble factor produced by alloantigen-activated spleen cells requires genetic homology between the factor-producing cells and responder cells in MLR. The ability of lymphocytes used as MLR responder cells to adsorb MLR suppressor factor was tested to investigate the expression of a receptor structure for suppressor molecules. Normal spleen or thymus cells had no effect on suppressor activity. Concanavalin A (Con A)-activated thymocytes, however, effectively removed suppressor activity, suggesting that the receptor is expressed only after activation and is not present or not functional on resting cells. Significantly neither phytohemagglutinin- nor lipopolysaccharide-activated lymphoid cells absorbed the factor. Furthermore, only Con A-activated thymocytes demonstrating genetic homology with the cell producing suppressor factor for H-2 regions to the right of I-E were effective absorbants. Alloantigen-stimulated spleen cells syngeneic to the suppressor cell also removed suppressor activity. These data support an hypothesis that subsequent to stimulation in MLR, T lymphocytes express a receptor, either through synthesis or alteration of an existing molecular structure, which then provides the appropriate site for interaction with suppressor molecules.

scholarly journals Monoclonal antibodies that recognize the product controlled by a gene in the I-J subregion of the mouse H-2 complex.

1981 ◽  
Vol 154 (5) ◽  
pp. 1290-1304 ◽  
Author(s):  
M Kanno ◽  
S Kobayashi ◽  
T Tokuhisa ◽  
I Takei ◽  
N Shinohara ◽  
...  
Keyword(s):  
T Cells ◽  
Monoclonal Antibodies ◽  
Keyhole Limpet Hemocyanin ◽  
Myeloma Cell ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Suppressor Activity ◽  
Petri Dishes ◽  
Thymus Cells ◽  
Specific Suppressor T Cells

The B cell hybridomas producing monoclonal antibodies (E10, D7, F4, H6, and D4) were established by the fusion of P3U1 or NS-1 murine myeloma cell lines and spleen cells of B10.A(5R) mice hyperimmunized with mitomycin C-treated B10.A(3R) spleen and thymus cells. Two types of monoclonal antibodies specific for the products controlled by a gene in the I-Jb subregion of the H-2 complex were characterized: one specific for the private type of I-Jb determinant, the other recognizing the cross-reactive determinant between the I-Jb and I-Jd products. By using these monoclonal reagents, the I-J-encoded product on the antigen-specific suppressor T cells was found to be expressed on their soluble suppressor factors. Furthermore, the I-Jb products were successfully detected not only on the T cell hybridoma with suppressor activity specific for keyhole limpet hemocyanin (KLH), but also on KLH-primed suppressor T cells enriched by antigen-coated petri dishes and concanavalin A-induced thymocyte blasts of C57BL/6 mice by complement-dependent cytotoxic assays and membrane fluorescence techniques.

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