scholarly journals Inhibition of T-antigen-binding cells by idiotypic antisera.

1977 ◽  
Vol 146 (3) ◽  
pp. 766-778 ◽  
Author(s):  
C A Prange ◽  
J Fiedler ◽  
D E Nitecki ◽  
C J Bellone
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Guinea Pig ◽  
T Cell Receptors ◽  
Binding Assay ◽  
T Antigen ◽  
Antigen Binding ◽  
Variable Regions ◽  
Heterologous System ◽  
Lymph Node Cells

Shared idiotypy between B- and T-cell receptors specific for the antigen L-tyrosine-p-azophenyltrimethylammonium [tyr(TMA)] was studied in an antigen-binding assay using idiotypic antisera. These idiotypic reagents were prepared by inoculation of rabbits with purified anti-tyr(TMA) antibody raised in strain 13 guinea pigs. The antisera blocked 78-83% of the antigen-binding T cells (T-ABC) and 50-55% of the antigen-binding B cells (B-ABC) from tyr(TMA)-immune strain 13 and outbred lymph node cells (LNC). An excess of normal guinea pig Ig in the ABC assay did not affect the ability of the idiotypic antisera to block T- and B-ABC. Nylon wool-passed tyr(TMA)-immune LNC were trypsin treated resulting in a 75% loss of T-ABC. The trypsin-treated population was then cultured for 16 h which resulted in a return of T-ABC to 92% of pretrypsin values. 77% of these regenerated T-ABC could be blocked with idiotypic antisera. Specificity of the idiotypic antisera was tested in L-tyrosine-p-azobenzenearsonate-immune guinea pig LNC. Neither T- nor B-ABC were blocked in this heterologous system. Further blocking experiments were performed to characterize the nature of the T-ABC receptor. A variety of anti-Ig reagents, some of which block B-ABC, do not inhibit T-ABC suggesting that variable regions on T cells are not linked to Ig Constant regions.

scholarly journals Differential Expression of Gamma Interferon mRNA Induced by Attenuated and Virulent Mycobacterium tuberculosis in Guinea Pig Cells after Mycobacterium bovis BCG Vaccination

2003 ◽  
Vol 71 (1) ◽  
pp. 354-364 ◽  
Author(s):  
Amminikutty Jeevan ◽  
Teizo Yoshimura ◽  
Kyeong Eun Lee ◽  
David N. McMurray
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Lymph Node ◽  
Amino Acid ◽  
Guinea Pig ◽  
Mrna Expression ◽  
Mycobacterium Bovis ◽  
Bcg Vaccination ◽  
Lymph Node Cells ◽  
Ifn Γ

ABSTRACT To determine whether Mycobacterium bovis BCG vaccination would alter gamma interferon (IFN-γ) mRNA expression in guinea pig cells exposed to Mycobacterium tuberculosis, we cloned a cDNA encoding guinea pig IFN-γ from a spleen cell cDNA library. The cDNA is composed of 1,110 bp, with an open reading frame encoding a 166-amino-acid protein which shows 56 and 41% amino acid sequence homology to human and mouse IFN-γ, respectively. Spleen or lymph node cells from naïve and BCG-vaccinated guinea pigs were stimulated with purified protein derivative (PPD) or M. tuberculosis H37Ra or H37Rv, and the total RNA was subjected to Northern blot analysis with a 32P-labeled probe derived from the cDNA clone. Compared to the IFN-γ mRNA expression in cells of naïve animals, that in spleen and lymph node cells exposed to various stimuli was enhanced after BCG vaccination. However, there was a significant reduction in IFN-γ mRNA levels when cells were stimulated with a multiplicity of infection of greater than 1 virulent M. tuberculosis bacterium per 10 cells. The enhanced IFN-γ mRNA response in BCG-vaccinated animals was associated with an increase in the proportions of CD4+ T cells in the spleens, as determined by fluorescence-activated cell sorter analysis. Furthermore, the nonadherent population in the spleens enriched either by panning with anti-guinea pig immunoglobulin G-coated plates or by purification on nylon wool columns produced more IFN-γ mRNA than whole spleen cells following stimulation with concanavalin A or PPD. This indicates that T cells are principally responsible for the upregulation of IFN-γ mRNA expression following BCG vaccination. The mechanism by which virulent mycobacteria suppress IFN-γ mRNA accumulation is currently under investigation.

scholarly journals Congenitally athymic nude (nu/nu) mice have Thy-1-bearing immunocompetent helper T cells in their peritoneal cavity.

1980 ◽  
Vol 151 (4) ◽  
pp. 965-968 ◽  
Author(s):  
H Ishikawa ◽  
K Saito
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Guinea Pig ◽  
Antibody Response ◽  
Sheep Erythrocyte ◽  
Helper T Cells ◽  
Spleen Cells ◽  
Lymph Node Cells ◽  
Pig Serum

Heavily irradiated peritoneal cells (PC) from congenitally athymic nude (nu/nu) mice markedly restored the impaired in vitro antibody response of nu/nu spleen cells to sheep erythrocyte antigens (T-dependent antigen), whereas irradiated spleen or lymph node cells from nu/nu mice had no effect on the response. This activity of the irradiated PC of nu/nu mice was completely abolished by treatment with anti-Thy-1.2 antiserum plus normal guinea pig serum (C') and is, therefore, attributable to a function of matured T cells.

scholarly journals Transfer of experimental allergic encephalomyelitis in Lewis rats using supernates of incubated sensitized lymph node cells.

1977 ◽  
Vol 145 (5) ◽  
pp. 1405-1410 ◽  
Author(s):  
C C Whitacre ◽  
P Y Paterson
Keyword(s):  
Spinal Cord ◽  
Lymph Node ◽  
Guinea Pig ◽  
Experimental Allergic Encephalomyelitis ◽  
Nervous Tissue ◽  
Allergic Encephalomyelitis ◽  
Lewis Rats ◽  
Transfer Activity ◽  
Lymph Node Cells ◽  
Experimental Allergic

Supernates derived from incubated lymph node cells of Lewis rats sensitized to guinea pig spinal cord-Freund's adjuvant transfer experimental allergic encephalomyelitis (EAE) to syngeneic recipients. EAE supernatant transfer activity (EAE-STA) is not demonstrable in supernates derived from LNC of control donors not sensitized to nervous tissue. After addition of brain antigen to active supernates, EAE-STA is not longer demonstrable.

scholarly journals Truncated mu (mu') chains in murine IgM. Evidence that mu' chains lack variable regions.

1985 ◽  
Vol 162 (6) ◽  
pp. 1862-1877 ◽  
Author(s):  
R Marks ◽  
M J Bosma
Keyword(s):  
Bone Marrow ◽  
Lymph Node ◽  
Molecular Mass ◽  
Tumor Cells ◽  
Isoelectric Focusing ◽  
Bone Marrow Cells ◽  
Normal Serum ◽  
Antigenic Determinants ◽  
Variable Regions ◽  
Lymph Node Cells

Secreted IgM was shown to contain truncated mu (mu') chains with an apparent molecular mass of approximately 55 kD. The estimated percentage of IgM heavy (H) chains in the mu' form ranged from less than or equal to 1% in the case of one tumor IgM protein (104E) to greater than or equal to 30% in normal serum IgM. Serum mu' chains lacked antigenic determinants characteristic of immunoglobulin variable regions and showed a restricted isoelectric focusing pattern compared with that of conventional mu chains. Intracellular mu' chains were readily detected in bone marrow cells but not in spleen or lymph node cells; mu' chains were also detected in IgM-producing tumor cells and in a hybridoma cell line that deleted its productive mu allele. These results predict irregularities in IgM structure and recall an old controversy concerning the valence of IgM molecules.

scholarly journals Massive upregulation of the Fas ligand in lpr and gld mice: implications for Fas regulation and the graft-versus-host disease-like wasting syndrome.

1995 ◽  
Vol 181 (1) ◽  
pp. 393-398 ◽  
Author(s):  
J L Chu ◽  
P Ramos ◽  
A Rosendorff ◽  
J Nikolić-Zugić ◽  
E Lacy ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Fas Ligand ◽  
Target Cells ◽  
Dependent Manner ◽  
Wasting Syndrome ◽  
Positive Target ◽  
Abnormal Cells ◽  
Lymph Node Cells ◽  
Fasl Mrna

Fas-deficient lpr and gld mice develop lymphadenopathy due to the accumulation of T cells with an unusual double negative (DN) (CD4-CD8-) phenotype. Previous studies have shown that these abnormal cells are capable of inducing redirected lysis of certain Fc receptor-positive target cells. Since the Fas ligand (FasL) has recently been shown to be partly responsible for T cell-mediated cytotoxicity, lymph node cells from lpr and gld mice were examined for the expression of FasL mRNA. Northern blot analysis revealed that lymph node cells obtained from lpr and gld mice had a striking increase in the level of expression of FasL mRNA predominantly due to expression in the DN T cells. Furthermore, lpr, but not gld lymph node cells killed the B cell line, A20, in a Fas-dependent manner. These findings indicate that Fas mutations result in a massive up-regulation of FasL which, most likely, results from repetitive exposure to (self) antigen. This phenomenon could explain the lpr-induced wasting syndrome observed when lpr bone marrow-derived cells are adoptively transferred to wild-type recipients.

Cytotoxic activity of guinea-pig lymph-node cells stimulatedin vitro

1978 ◽  
Vol 22 (5) ◽  
pp. 595-601 ◽  
Author(s):  
Amnon Altman ◽  
Herbert J. Rapp
Keyword(s):  
Lymph Node ◽  
Guinea Pig ◽  
Cytotoxic Activity ◽  
Lymph Node Cells

scholarly journals OCCURRENCE OF DELAYED HYPERSENSITIVITY DURING THE DEVELOPMENT OF ARTHUS TYPE HYPERSENSITIVITY

1958 ◽  
Vol 107 (1) ◽  
pp. 109-124 ◽  
Author(s):  
S. B. Salvin ◽  
Keyword(s):  
Lymph Node ◽  
Guinea Pig ◽  
Latent Period ◽  
Guinea Pigs ◽  
Specific Antigen ◽  
Egg Albumin ◽  
Lymph Node Cells ◽  
Type Inclusion ◽  
Antibody Determination ◽  
Circulating Antibody

Guinea pigs were injected in the footpads with either purified diphtheria toxoid or recrystallized egg albumin in Freund adjuvant without mycobacteria. Each guinea pig was then skin-tested only once with the specific antigen and bled for antibody determination. After injection of the sensitizing antigen, a latent period occurred during which neither sensitivity nor circulating antibody could be detected. A period of delayed sensitivity followed wherein circulating antibody could not be discerned and which could be transferred by lymph node cells. Ultimately, the Arthus type sensitivity developed, accompanied by circulating antibody. The duration and severity of reactions to homologous antigens during the last 2 phases varied with the antigen and with the dose. An increase in the sensitizing dose decreased the duration of the delayed type of allergy, a decrease in the dose prolonged the delayed type. Inclusion of mycobacterium in the sensitizing inoculum tended to introduce delayed sensitivity earlier and delay the onset of Arthus type sensitivity. When specific precipitate in antibody excess was included with the toxoid in the sensitizing dose, the onset of the Arthus phase was hastened. When lymph nodes from a large number of sensitized donors were removed during the latter part of the latent period, recipients of the cells showed a delayed type sensitivity.

scholarly journals Properties of reticulum cell sarcomas in SJL/J mice. V. Nature of reticulum cell sarcoma surface antigen which induces proliferation of normal SJL/J T cells.

1977 ◽  
Vol 146 (1) ◽  
pp. 132-145 ◽  
Author(s):  
N M Ponzio ◽  
C S David ◽  
D C Shreffler ◽  
G J Thorbecke
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Lymphocytes ◽  
Tumor Cells ◽  
Proliferative Response ◽  
Reticulum Cell ◽  
Reticulum Cell Sarcoma ◽  
Cell Surface Antigens ◽  
Cell Sarcoma ◽  
Lymph Node Cells

The results of studies on the reticulum cell sarcoma (RCS) tumors of SJL/J mice presented here, indicate that spontaneous tumors, which arise in older mice, also possess the capacity to induce the vigorous proliferative response in syngenetic T lymphocytes that are characteristic of the transplantable RCS lines. Analysis of cell surface antigens revealed the presence of Ia determinats on gradient-purified transplantable RCS tumor cells; however, these cells did not express Thy 1.2, nIg, or, any of the viral proteins that were tested for by specific antisera. Pretreatment of RCS cells with anti-Ia sera and complement-deleted cells that were stimulatory for syngenetic T lymphocytes, and addition of anti-Ia sera directly to cultures blocked the proliferative response at the stimulator (RCS) cell level. Lymph node cells from H-2(8) strains other than SJL/J, including A.SW and B10.S also gave proliferative responses to RCS cells, although lower in magnitude. A requirement on the part of responding cells for identity with RCS cells at the Ir region was indicated by the finding that A.TH but not A.TL lymph node cells responded to RCS. It is concluded that RCS cells stimulate Ir-region identical T cells (without evidence of presensitization) through a modification in the expression of Ia antigens on the surface of the tumor cells.

scholarly journals The Substrate-Binding Domain of 21-Hydroxylase, the Main Autoantigen in Autoimmune Addison’s Disease, Is an Immunodominant T Cell Epitope

Endocrinology ◽  
2006 ◽  
Vol 147 (5) ◽  
pp. 2411-2416 ◽  
Author(s):  
Eystein S. Husebye ◽  
Eirik Bratland ◽  
Geir Bredholt ◽  
Mati Fridkin ◽  
Molly Dayan ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Cell ◽  
Proliferative Response ◽  
Substrate Binding ◽  
Cell Epitope ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Adrenal Failure ◽  
Lymph Node Cells

The steroidogenic enzyme 21-hydroxylase (21OH) is the main autoantigen in autoimmune primary adrenal failure (Addison’s disease). Autoantibodies against 21OH are immunological markers of an ongoing autoimmune process but are not directly involved in the tissue destruction. Autoreactive T cells are thought to mediate tissue damage, but the T cell antigen(s) has not been identified. To find out whether 21OH contains important immunodominant epitopes for T cells, we first immunized BALB/c and SJL inbred mouse strains with recombinant 21OH and showed that lymph node cells proliferated effectively following in vitro stimulation with recombinant 21OH (stimulation indices (SI) 20–40). We further synthesized a series of peptides based on 21OH with amino acid sequences with propensity to bind to major histocompatibility complex class II molecules. Only a few peptides could trigger lymphocytes of 21OH-primed mice to proliferate. One of these, 21OH (342–361), stimulated effectively 21OH-primed lymph node cells of SJL mice (SI = 4–8) and also, although to a lesser extent, of BALB/c mice (SI = 2.5). When SJL mice were immunized with 21OH (342–361), the immunizing peptide as well as peptide 21OH (346–361) triggered a significant proliferative response (SI = 24). A peptide from another part of 21OH, namely 21OH (191–202), did not stimulate the 21OH (342–361)-primed cells. Moreover, stimulation of lymph node cells of mice immunized with 21OH (342–361) with 21OH resulted in a significant proliferative response. We conclude that 21OH (342–361) is an immunodominant determinant for T cells in SJL and probably BALB/c mice. 21OH (342–361) corresponds to the substrate binding site of the enzyme. The p342–361 region may be involved in the pathogenesis of autoimmune adrenal failure in humans.

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