scholarly journals T-cell-specific murine Ia antigens: serology of I-J and I-E subregion specificities.

1978 ◽  
Vol 148 (3) ◽  
pp. 692-703 ◽  
Author(s):  
C E Hayes ◽  
F H Bach
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Concanavalin A ◽  
Lymphocyte Activation ◽  
Antigenic Determinants ◽  
Spleen Cells ◽  
Cell Reactivity ◽  
Functional Studies ◽  
Lymph Node Cells ◽  
T Cell Subpopulations

(B10 X B10.D2)F1 mice were immunized with B10.A(5R) concanavalin A-stimulated thymocyte blasts. The genetic disparity between donor and recipient was restricted to the I-J and I-E subregions of the murine major histocompatibility (H-2) complex. A high-titered, T-cell-specific anti I-JkEk serum was obtained. The antiserum lysed 27-30% of haplotype k, q, or s lymph node cells, 5.3 +/- 2% of haplotype k spleen cells, and did not lyse thymocytes. Nylon wool-passed lymph node or spleen cells (H-2k) showed considerable reactivity with anti-I-JkEk serum (35-40% lysis); anti-Thy1.2 plus complement-treated spleen cells did not react (less than 5% lysis). I-Ek antibody was detected by B10.A(3R) lymph node cell reactivity (20% lysis), whereas reaction with H-2k lymph node cells after B10.A(3R) absorption demonstrated IJk antibody (12% lysis). Lymphocyte activation with alloantigen or mitogen led to increased anti-I-JkEk serum reactivity. These results, showing antibody production to at least two T-cell Ia antigenic determinants by concanavalin A thmocyte blast immunization, suggest that a group of I-region-encoded T-cell specificities may not have been detected using conventional immunization protocols because they would not have comprised a major antigenic component of the immunizing cell population. The existence of multiple Ia antigenic determinants unique to T lymphocytes would have important implications for serological and functional studies of T-cell subpopulations.

scholarly journals The capacity of mitogen-responsive T cells to home to their tissue of origin, analyzed by means of chromosome markers

1976 ◽  
Vol 143 (3) ◽  
pp. 660-671 ◽  
Author(s):  
MJ Doenhoff ◽  
AJS Davies
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Concanavalin A ◽  
Spleen Cells ◽  
Con A ◽  
Syngeneic Mouse ◽  
Lymph Node Cells ◽  
Mitogen Responsiveness ◽  
Tissue Of Origin ◽  
Syngeneic Recipient

Lance and Taub (1) showed that when radioactively labeled lymphocytes were injected into a syngeneic mouse and the lymph node cells of this animal transferred to a second syngeneic recipient, the proportion of radioactivity found in the lymph node relative to the amount present in the spleen of the secondary recipient had increased markedly. The interpretation of this result was that some lymphocytes have the capacity to home to their organ of origin. The purpose of the experiments described here was to test the homing copacity of T cells by a method that did not involve radioactive labeling. It has been shown elsewhere that some or all mouse T cells are stimulated to divide in culture by the mitogens phytohemagglutinin (PHA) and concanavalin A (Con A) (2). We therefore elected to inject karyotypically distinct lymphocytes into syngeneic recipients and to follow their subsequent distribution by culture of lymph node and spleen cells of the recipient with PHA or Con A. In this manner the homing capacities of spleen and lymph node T cells could be determined, and furthermore, the effects of labeling with chromium-51 ((51)Cr) could be assayed with respect to the persistence of mitogen responsiveness in the injected cells.

scholarly journals THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES

1973 ◽  
Vol 137 (4) ◽  
pp. 1042-1059 ◽  
Author(s):  
Maja Nowakowski ◽  
Joseph D. Feldman ◽  
Shogo Kano ◽  
Barry R. Bloom
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Guinea Pig ◽  
B Cell ◽  
Vesicular Stomatitis Virus ◽  
Mouse Spleen ◽  
Spleen Cells ◽  
Lymph Node Cells ◽  
Vesicular Stomatitis ◽  
Number Of Cells

A variety of lymphoid cell populations were examined in terms of their ability to replicate vesicular stomatitis virus (VSV), a lytic, RNA-containing virus maturing at the cell surface. The number of cells capable of producing VSV was estimated in terms of infectious centers by the virus plaque assay (VPA), and morphologically by electron microscopy (EM). The lymphoid cells examined in this study included: (a) lymph node cells from delayed hypersensitive guinea pigs stimulated by specific antigen, (b) mouse spleen cells activated by selective bone marrow-derived (B) cell and thymus derived (T) cell mitogens, and (c) cells of human and murine continuous lymphoblastoid or lymphoma lines. In unstimulated cultures of guinea pig lymph node cells there is a background of approximately 1 in 1,000 cells which produces VSV; in purified protein derivative (PPD)-stimulated cultures the number of cells producing virus was 1.6% in the VPA and 1.9% by EM. These cells were large lymphocytes with some morphological features of transformed lymphocytes but were not typical blast cells. A few macrophages were associated with virus in both stimulated and control cultures. These observations indicate that (a) cells responsive to antigens, as detected by a marker virus, were lymphocytes; (b) cells other than lymphocytes (macrophages) were capable of replicating VSV even without antigenic stimulation; and (c) the correlation of results obtained by VPA and morphologic examination was usually quite good. Of the total number of mouse spleen cells stimulated with concanavalin (Con A), a T cell mitogen, 4.5 (EM)–5.7% (VPA) were associated with VSV. These were characteristic transformed lymphocytes, similar to phytohemagglutinin (PHA)-stimulated human lymphocytes. In contrast Escherichia coli lipopolysaccharide (LPS)-treated mouse spleen cultures contained lower numbers of virus plaque-forming cells. The majority of such cells associated with virus displayed extensive rough endoplasmic reticulum. Two cultured murine lymphomas containing lymphocytes with the θ surface marker (L5178Y and EL-4) showed a 15–100-fold higher incidence of virus-producing cells than leukemias (L1210 and C57Bl/6) which did not carry this marker. Similarly, the L2C guinea pig leukemia, a known B cell leukemia, yielded a low percent of virus plaque-forming cells (<2%). However, MOPC-104, a plasma cell tumor presumed to be of B cell origin, was found to be an efficient virus producer. There was a wide variation in the efficiency of VSV replication among human lymphoblastoid lines. One line, Wil-2, produced 80% infectious centers after 24 h of exposure to VSV, and all cells were associated with virus at the EM level. The relationship between the virus-producing cells and different lymphocyte subpopulations as well as the efficiency of the two assays for studying virus-producing lymphocytes is discussed.

scholarly journals A MOUSE B-CELL ALLOANTIGEN DETERMINED BY GENE(S) LINKED TO THE MAJOR HISTOCOMPATIBILITY COMPLEX

1973 ◽  
Vol 138 (6) ◽  
pp. 1289-1304 ◽  
Author(s):  
David H. Sachs ◽  
James L. Cone
Keyword(s):  
Major Histocompatibility Complex ◽  
Lymph Node ◽  
T Cell ◽  
B Cells ◽  
Cell Surface ◽  
B Cell ◽  
Surface Antigen ◽  
Major Histocompatibility ◽  
Spleen Cells ◽  
Histocompatibility Complex

Antibodies cytotoxic for only a subpopulation of C57Bl/10 lymph node and spleen cells were detected when rat antiserum against B10.D2 was exhaustively absorbed with B10.A lymphocytes. Antibodies of similar specificity were also detected in B10.A anti-B10.D2 and in B10.A anti-C57Bl/10 alloantisera. Reactions with recombinant strains of mice indicate that the cell-surface antigen(s) responsible for this specificity is determined by gene(s) in or to the left of the Ir-1 region of the major histocompatibility complex. A variety of criteria implicate B cells as the subpopulation of lymphocytes bearing this antigen. In view of these data and the recent report by others of a T-cell alloantigen determined by gene(s) in the major histocompatibility complex, it seems possible that there may be a variety of H-2-linked alloantigens expressed preferentially on subclasses of lymphocytes.

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.

Tumour rejection after adoptive transfer of line-10-immune spleen cells is mediated by two T cell subpopulations

1991 ◽  
Vol 34 (2) ◽  
pp. 103-110 ◽  
Author(s):  
P. A. Steerenberg ◽  
E. Geerse ◽  
W. H. De Jong ◽  
R. Burger ◽  
R. J. Scheper ◽  
...  
Keyword(s):  
T Cell ◽  
Adoptive Transfer ◽  
Spleen Cells ◽  
Tumour Rejection ◽  
Cell Subpopulations ◽  
T Cell Subpopulations ◽  
Immune Spleen Cells

scholarly journals A cell-mediated reaction against glomerular-bound immune complexes.

1979 ◽  
Vol 150 (6) ◽  
pp. 1410-1420 ◽  
Author(s):  
A K Bhan ◽  
A B Collins ◽  
E E Schneeberger ◽  
R T McCluskey
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Immune Complexes ◽  
Gamma Globulin ◽  
Mononuclear Phagocytes ◽  
A Cell ◽  
Lymph Node Cells ◽  
Soluble Immune Complexes ◽  
Histologic Changes ◽  
Glomerular Capillaries

Lewis rats were given a single i.v. injection of soluble immune complexes containing human serum albumin (HSA) and rabbit anti-HSA antibodies, prepared in antigen excess. This resulted in localization of HSA and rabbit gamma globulin (RGG) in glomerular mesangial regions without producing definite histologic changes. 24 h after the injection of immune complexes, groups of these rats received lymph node cells or T-cell preparations from syngeneic donors sensitized to RGG, HSA, or ovalbumin; another group received no cells. All of these groups and a group of normal control rats were given injections of [3H]thymidine at 18, 27, and 44 h. The animals were killed 48 h after the time of cell transfer. In histologic sections, glomerular abnormalities were found only in some of the animals that had received immune complexes and lymph node cells or T-cell populations from donors sensitized to HSA or RGG; the lesions were characterized by focal and segmental increase in cells in mesangial regions. Autoradiographs revealed significantly greater numbers of labeled cells in mesangial regions and glomerular capillaries in the groups that had received immune complexes and cells from HSA- or RGG-sensitized donors than in any of the other groups. Electronmicroscopic studies suggested that the increase in cellularity in mesangial regions resulted from an influx of mononuclear phagocytes. The findings indicate that cell-mediated reactions can be initiated by the interaction between sensitized T lymphocytes and antigens present in immune complexes within mesangial regions.

scholarly journals SYNERGY AMONG LYMPHOID CELLS MEDIATING THE GRAFT-VERSUS-HOST RESPONSE

1972 ◽  
Vol 135 (5) ◽  
pp. 1059-1070 ◽  
Author(s):  
Robert E. Tigelaar ◽  
Richard Asofsky
Keyword(s):  
Lymph Node ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Blood Leukocytes ◽  
Graft Versus Host ◽  
Average Survival ◽  
Lymph Node Cells ◽  
The One ◽  
Kinetics Of ◽  
Cell Inoculum

A mortality assay was used to quantitate graft-versus-host (GVH) reactions in sublethally irradiated (400 R) neonatal (C57BL/6 x BALB/c)F1 recipients of BALB/c lymphoid cells from various tissues. The probit of the 35 day cumulative per cent of mortality was a linear function of the logarithm of the cell inoculum for any tissue; reactivities of different tissues fell on a series of parallel lines. Peripheral blood leukocytes (PBL), the most active cells, were about 30 times as active as thymocytes, the least active cells studied; femoral lymph node cells and spleen cells were about 23 and 8 times as reactive as thymocytes, respectively. The average survival time of recipients of thymocytes who eventually died was nearly a week longer than that of recipients of comparably lethal numbers of PBL, lymph node, or spleen cells. Mixtures of PBL and thymocytes gave levels of 35 day mortality significantly greater than those expected if the reactivities of the mixture had been merely the sum of the reactivities of the components measured separately, thereby confirming in any assay independent of host splenomegaly the synergistic interaction of thymocytes and PBL in the GVH reaction. Both populations of cells in the mixture had to be allogeneic to the host in order to observe this synergy. The kinetics of cumulative mortality observed for mixtures of PBL and thymocytes were indistinguishable from those seen with thymocytes alone, indicating activation of the latter cell type. Finally, comparison of the relative abilities of different cell populations to cause splenomegaly on the one hand and lethal runting on the other has raised the possibility that expression of different effector functions of cell-mediated immune reactions may in fact be initiated by distinct cells.

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