scholarly journals ANTIBODY AND IMMUNOGLOBULIN PRODUCTION AT THE CELLULAR LEVEL IN BURSECTOMIZED-IRRADIATED CHICKENS

1969 ◽  
Vol 129 (6) ◽  
pp. 1247-1259 ◽  
Author(s):  
Gunnar V. Alm ◽  
Raymond D. A. Peterson
Keyword(s):  
Plasma Cells ◽  
Rabbit Antiserum ◽  
Later Life ◽  
Primary Response ◽  
Lymphoid Cells ◽  
Primary Immune Response ◽  
Antigenic Determinants ◽  
Spleen Cells ◽  
Lymphoid Cell Population

The effect of bursectomy combined with sublethal X-irradiation in the newly hatched chicken on the immunoglobulin and antibody producing capacity in later life was investigated. The previous findings of a significant incidence of hypogammaglobulinemia in such animals were confirmed. Spleen cells from severely hypogammaglobulinemic animals synthesized and secreted little or no immunoglobulin. Such spleen lymphoid cells contained fewer immunoglobulin antigenic determinants than spleen cells from irradiated control animals as evidenced by their relative inability to respond by an increased DNA synthesis after in vitro culture with rabbit antiserum to chicken immunoglobulin. Therefore, the deficiency in the immunoglobulin synthesis extends not only to actively secreting cells such as plasma cells, but to the entire lymphoid cell population. As expected, most irradiated-bursectomized chickens, irrespective of plasma immunoglobulin levels failed to produce detectable amount of circulating antibodies to Brucella abortus antigen in the primary immune response. Severely hypogammaglobulinemic animals were completely unable to elaborate any plaque forming cells (PFC) in the primary response to sheep red blood cells (SRBC). The results of this investigation support the contention that in the severely hypogammaglobulinemic bursectomized-irradiated chicken the entire antibody producing and immunoglobulin producing cell line is absent. The possibility remains that precursor or stem cells are present but are not appropriately directed to antibody synthesis by other cell types.

scholarly journals CYTOTOXICITY BY NONIMMUNE ALLOGENEIC LYMPHOID CELLS

1967 ◽  
Vol 126 (2) ◽  
pp. 395-405 ◽  
Author(s):  
Erna Möller
Keyword(s):  
Lymphoid Cells ◽  
Primary Immune Response ◽  
Antigenic Determinants ◽  
Target Cells ◽  
Mouse Tumor ◽  
Hybrid Cells ◽  
F1 Hybrid ◽  
Target Strain ◽  
Immune Response In Vitro

Nonimmune lymphoid cells were capable of causing cytotoxicity of H-2 incompatible mouse tumor cells in vitro in the presence of PHA, whereas syngeneic cells were not. Semisyngeneic and X-irradiated (1500–3000 R) F1 hybrid lymphoid cells were cytotoxic for target cells derived from one of the parental strains. In addition, parental nonimmune and X-irradiated lymphoid cells damaged hybrid target cells. It was concluded that one component of cytotoxicity was not related to an induction of a primary immune response in vitro, since F1 hybrid cells are not capable of reacting immunologically against parental type target cells. It seemed probable that cytotoxicity was caused by target cell confrontation with antigenically and/or structurally incompatible lymphoid cells. This conclusion was strengthened by the demonstration that isoantibodies produced in the target strain and directed against the allogeneic lymphoid cells specifically suppressed cytotoxicity. Isoantibodies reacting against some but not all of the antigenic determinants of the lymphoid cells differentiating them from the target cells did not suppress cytotoxicity. The specific suppression of cytotoxicity by specific isoantibodies against the lymphoid cells support the allogeneic inhibition concept.

scholarly journals CELL INTERACTIONS IN THE PRIMARY IMMUNE RESPONSE IN VITRO: A REQUIREMENT FOR SPECIFIC CELL CLUSTERS

1969 ◽  
Vol 129 (2) ◽  
pp. 351-362 ◽  
Author(s):  
Donald E. Mosier
Keyword(s):  
Immune Response ◽  
Cell Cultures ◽  
Primary Immune Response ◽  
Antigenic Determinants ◽  
Specific Cell ◽  
Spleen Cells ◽  
Sheep Erythrocytes ◽  
Cell Clusters ◽  
Immune Response In Vitro

Mouse spleen cells were found to associate in cell clusters during the primary immune response to sheep erythrocytes in vitro. About 10% of the cell clusters had the following unique properties; (a) they contained most, if not all, antibody-forming cells, (b) they contained only cells forming antibody to one antigen when cell cultures were immunized with two antigens, (c) the cells in clusters reaggregated specifically after dispersion, and (d) the specific reaggregation of clusters appeared to be blocked by antibody to the antigen. The integrity of cell clusters was required for the proliferation of antibody-forming cells, and prevention of clustering by mechanical means or by excess antibody blocked the immune response. Antibody and antigenic determinants on the surfaces of cells probably provide the basis for interaction. The unique microenvironment of cell clusters was essential for the primary immune response in vitro.

scholarly journals Vaccination-induced variation in the 140 kD merozoite surface antigen of Plasmodium knowlesi malaria.

1987 ◽  
Vol 165 (2) ◽  
pp. 359-367 ◽  
Author(s):  
F W Klotz ◽  
D E Hudson ◽  
H G Coon ◽  
L H Miller
Keyword(s):  
Monoclonal Antibodies ◽  
Malaria Infection ◽  
Rhesus Monkeys ◽  
Plasmodium Knowlesi ◽  
Rabbit Antiserum ◽  
Antigenic Determinants ◽  
Partial Protection ◽  
Erythrocyte Invasion ◽  
Merozoite Surface Antigen

Immunity to 143/140 kD schizont antigens of a monkey malaria, Plasmodium knowlesi, provides partial protection to lethal malaria infection in rhesus monkeys challenged with uncloned parasites. To determine the capacity of a cloned parasite to generate variants of the 143/140 kD antigens, immunized monkeys were challenged with a clone of P. knowlesi. Parasites recovered 8 d after inoculation with a cloned parasite retained the 143/140 kD antigens. Parasites recovered 30 d after challenge had undergone changes in the 143/140 kD antigens. Antibodies that block erythrocyte invasion in vitro of the inoculum parasites did not inhibit invasion of erythrocytes by two isolates recovered from the immunized monkeys. An isolate from one monkey recovered on day 30 contained clones expressing new 76/72 kD antigens reactive with rabbit antiserum against the 143/140 kD proteins, and other clones expressing no antigens crossreactive with antisera against the 143/140 kD proteins. An isolate from another monkey obtained 59 d after challenge expressed new antigens of 160/155, 115/113, and 87/85 kD. Using monoclonal antibodies, we found that epitopes were lost from the variant proteins, but we were unable to determine whether new epitopes had appeared. We conclude that clones of P. knowlesi can rapidly vary antigenic determinants on the 143/140 kD proteins in animals immunized with these antigens.

scholarly journals HORMONE-LIKE ACTIVITY OF A THYMUS HUMORAL FACTOR ON THE INDUCTION OF IMMUNE COMPETENCE IN LYMPHOID CELLS

1974 ◽  
Vol 139 (1) ◽  
pp. 193-207 ◽  
Author(s):  
Abraham I. Kook ◽  
Nathan Trainin
Keyword(s):  
Adenyl Cyclase ◽  
Lymphoid Cells ◽  
Humoral Factor ◽  
Flufenamic Acid ◽  
Intracellular Camp ◽  
Immune Competence ◽  
Dibutyryl Camp ◽  
Spleen Cells ◽  
Antigenic Challenge

Experiments reported here were performed to understand the mechanism by which THF increases the immunocompetence of spleen cells from NTx mice. Dibutyryl cAMP or substances which increase intracellular levels of cAMP in lymphocytes such as Poly(A:U), theophylline, or PGE2 were shown to mimic the effect of THF and confer reactivity in an in vitro GvH response to spleen cells from NTx mice. Flufenamic acid, an antagonist to PGE2, was shown to inhibit the induction of competence by this substance. It was found that THF induces competence by activating membranal adenyl cyclase which leads to a rise in intracellular cAMP in thymus-derived cells only. These biochemical changes occur before antigenic stimulation and are unrelated to antigenic challenge. These findings indicate that THF exerts its effect via cAMP and are in agreement with the concepts which permit to classify THF as a thymus hormone.

scholarly journals Comparative studies on monotypic IgM lambda and IgG kappa from an individual patient. IV. Immunofluorescent evidence for a common clonal synthesis

Blood ◽  
1977 ◽  
Vol 50 (2) ◽  
pp. 203-211 ◽  
Author(s):  
JE Hopper
Keyword(s):  
Plasma Cells ◽  
Lymphoproliferative Disorders ◽  
Lymphoid Cells ◽  
Antigenic Determinants ◽  
Sequence Analyses ◽  
Gamma Chain ◽  
Heavy Chains ◽  
Broad Implication ◽  
Clonal Origin ◽  
Immunofluorescent Analysis

Abstract Previous studies have presented evidence of shared idiotypic antigenic determinants located within the variable (VH) region of the heavy chains of monotypic IgMlambda and IgGkappa isolated from the serum of an individual patient, Bro, with Waldenstrom macroglobulinemia. Comparative N-terminal VH sequence analyses have demonstrated that the respective micron and gamma chains belong to separate VH subgroups. The entire VH sequence of the Bro micron chain has been reported, but the VH sequence of the Bro gamma chain still awaits completion. We report the results of an immunofluorescent analysis of cytoplasmic Ig of lymphoid cells isolated from the patient's peripheral blood and bone marrow. Between 6% and 9% of the cytoplasmic Ig-positive lymphoid cells exhibited fluorescent evidence for the dual presence of kappa and lambda chains are well as micron and gamma chains. These results strongly suggest that the idiotypically related Bro IgMlambda and IgGkappa paraproteins are derived from a common clonal origin. Moreover, these findings extend the results of a previous study that has demonstrated the dual presence of IgGkappa and IgGlambda paraproteins within individual myeloma plasma cells. Collectively, these studies suggest that a single neoplastic lymphoid clone may not necessarily be restricted to the synthesis of Ig proteins of the identical light chain class. These findings may have a broad implication for the understanding of surface and cytoplasmic Ig markers of neoplastic lymphoid cells in certain other lymphoproliferative disorders.

scholarly journals Interaction of the v-Rel oncoprotein with NF-kappaB and IkappaB proteins: heterodimers of a transformation-defective v-Rel mutant and NF-2 are functional in vitro and in vivo.

1996 ◽  
Vol 16 (3) ◽  
pp. 1169-1178 ◽  
Author(s):  
D W White ◽  
G A Pitoc ◽  
T D Gilmore
Keyword(s):  
Dna Binding ◽  
Protein Interactions ◽  
Cellular Protein ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Nf Kappa B ◽  
I Kappa B Alpha ◽  
Chicken Spleen

The v-Rel oncoprotein of the avian Rev-T retrovirus is a member of the Rel/NF-kappa B family of transcription factors. The mechanism by which v-Rel malignantly transforms chicken spleen cells is not precisely known. To gain a better understanding of functions needed for transformation by v-Rel, we have now characterized the activities of mutant v-Rel proteins that are defective for specific protein-protein interactions. Mutant v-delta NLS, which has a deletion of the primary v-Rel nuclear localizing sequence, does not interact efficiently with I kappa B-alpha but still transforms chicken spleen cells approximately as well as wild-type v-Rel, indicating that interaction with I kappa B-alpha is not essential for the v-Rel transforming function. A second v-Rel mutant, v-SPW, has been shown to be defective for the formation of homodimers, DNA binding, and transformation. However, we now find that v-SPW can form functional DNA-binding heterodimers in vitro and in vivo with the cellular protein NF-kappa B p-52. Most strikingly, coexpression of v-SPW and p52 from a retroviral vector can induce the malignant transformation of chicken spleen cells, whereas expression of either protein alone cannot. Our results are most consistent with a model wherein Rel homodimers or heterodimers must bind DNA and alter gene expression in order to transform lymphoid cells.

scholarly journals IMMUNOCOMPETENCE OF SPLEEN CELLS FROM NEONATALLY THYMECTOMIZED MICE CONFERRED IN VITRO BY A SYNGENEIC THYMUS EXTRACT

1969 ◽  
Vol 130 (4) ◽  
pp. 765-775 ◽  
Author(s):  
Nathan Trainin ◽  
Myra Small ◽  
Amiela Globerson
Keyword(s):  
Host Response ◽  
Protein Concentration ◽  
Lymphoid Cells ◽  
Immune Reactivity ◽  
Spleen Cells ◽  
Graft Versus Host ◽  
Thymus Extract ◽  
Adult Mice ◽  
Thymectomized Mice

Impaired immunological competence of spleen cells from neonatally thymectomized C57B1/6 young adult mice was apparent when these cells were tested in an in vitro graft-versus-host assay. Spleen cell inocula prepared from thymectomized mice did not induce enlargement of (C3H/eb x C57BI/6)F1 newborn spleen explants, whereas the same number of cells from intact donors consistently initiated splenomegaly. Spleen enlargement was observed, however, when the explants were challenged by cells from thymectomized donors in the presence of syngeneic thymus extract, indicating that the spleen cells in suspension attained immunological competence under the influence of a non-cellular component of the thymus. Immunocompetence was also evident when the cells from thymectomized donors were first incubated with thymus extract for 1 hr and subsequently tested for reactivity. Cells from the same thymectomized donor mice exposed in parallel to extracts from syngeneic spleen or mesenteric lymph node at an equivalent protein concentration did not initiate a graft-versus-host response. These experiments demonstrate that immune reactivity in the graft-versus-host response involves activation of lymphoid cells by a humoral factor of the thymus acting directly upon these cells.

scholarly journals IgE class-restricted tolerance induced by neonatal administration of soluble or cell-bound IgE. Cellular mechanisms.

1984 ◽  
Vol 160 (4) ◽  
pp. 953-970 ◽  
Author(s):  
S S Chen ◽  
F T Liu ◽  
D H Katz
Keyword(s):  
Tolerance Induction ◽  
Suppressor Cells ◽  
Mouse Cell ◽  
Lymphoid Cells ◽  
Soluble Form ◽  
Antigenic Determinants ◽  
Antigen Specificity ◽  
Cellular Mechanisms ◽  
Neonatal Treatment

Certain aspects of the phenomenon of IgE class-restricted tolerance induced in mice by neonatal treatment with monoclonal IgE, either in soluble form or coupled to syngeneic spleen cells, were examined. The present studies document that this tolerance results from exposure to IgE molecules, irrespective of their antigen specificity, and the resulting effects are polyclonal in nature since IgE responses directed against antigenic determinants unrelated to the tolerance-inducing IgE molecules are affected. Moreover, such findings indicate that the molecular subregion(s) responsible for inducing IgE class-restricted tolerance resides in the epsilon heavy chain constant region domain(s) of IgE. When soluble IgE is employed, tolerance induction results from neonatal treatment with doses as low as 2.5 micrograms per injection per mouse; cell-bound IgE is considerably more potent, in terms of total dose required, since tolerance results from treatment with as few as 1 X 10(6) cells per injection (per mouse), equivalent to an absolute quantity of 0.2 ng of IgE per injection. This long-term class-specific tolerance appears to be a unique feature of the IgE antibody system, since treatment of mice with monoclonal antibodies of the IgA, IgG1, or IgG2b isotypes, either in soluble or cell-bound form, does not perturb antibody responses of their corresponding isotypes or in the IgE class. By analyzing the lymphoid cells of IgE-tolerant mice after they reached adulthood, the following observations were made: (a) lymphoid cells from such tolerant mice fail to develop FcR epsilon + cells upon in vitro stimulation with IgE, as is characteristically observed with lymphoid cells from nontolerant mice; and (b) mice rendered tolerant by neonatal treatment with soluble IgE possess IgE class-restricted suppressor T cells, demonstrable in adoptive transfer experiments, whereas no such suppressor cells are evident in mice in which cell-bound IgE was used for neonatal treatment. The latter observations could mean that two different mechanisms underlie the IgE class-restricted tolerance, or both mechanisms operate coordinately to varying degrees depending upon which regimen is used for tolerance induction, as discussed herein.

scholarly journals GENERATION OF CYTOTOXIC T LYMPHOCYTES IN VITRO

1974 ◽  
Vol 140 (3) ◽  
pp. 718-730 ◽  
Author(s):  
H. Robson MacDonald ◽  
Howard D. Engers ◽  
Jean-Charles Cerottini ◽  
K. Theodor Brunner
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Primary Response ◽  
Target Cells ◽  
Spleen Cells ◽  
Response Curves ◽  
Specific Cytotoxicity ◽  
Allogeneic Stimulation ◽  
Ctl Activity

Mouse cytotoxic T lymphocytes (CTL) were generated in unidirectional mixed leukocyte cultures (MLC) using normal C57BL/6 spleen cells as responding cells and irradiated DBA/2 spleen cells as stimulating cells. Cytotoxicity was assayed on 51Cr-labeled P-815 (DBA/2) target cells, and the relative frequency of CTL in individual cell populations was estimated from dose-response curves. Upon inclusion of 2-mercaptoethanol in the culture medium, it was found that significant CTL activity could be detected for as long as 3 wk in primary MLC. Reexposure of MLC cells to the original stimulating alloantigens after 14–41 days in culture resulted in significant cell proliferation and rapid regeneration of high levels of immunologically specific cytotoxicity. CTL activity in these secondary cultures increased dramatically within the first 24 h and reached higher peak levels than those found at the peak of the primary response. Furthermore, proliferation and reappearance of CTL activity could be demonstrated following each of as many as four sequential alloantigenic stimulations of the same initial cell population at 20-day intervals. Interestingly, cells recovered from MLC at the peak of the primary response on day 4 were insensitive to further allogeneic stimulation. Taken together, these results are consistent with the hypothesis that CTL differentiate in MLC to become long-lived memory cells which gradually lose their cytotoxic activity. Upon reexposure to specific alloantigen, such memory CTL rapidly regain their functional activity and proliferate to generate an expanded CTL population.

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