Antigen-specific augmentation of delayed-type hypersensitivity by a humoral factor in the culture supernatant of immune spleen cells

1984 ◽  
Vol 84 (1) ◽  
pp. 206-209 ◽  
Author(s):  
Akira Yamada ◽  
Kunisuke Himeno ◽  
Yoshio Kumazawa ◽  
Kikuo Nomoto
Keyword(s):  
Culture Supernatant ◽  
Humoral Factor ◽  
Delayed Type Hypersensitivity ◽  
Spleen Cells ◽  
Immune Spleen Cells

scholarly journals Therapy of a fatal murine cytomegalovirus infection with thymic humoral factor (THF-γ2) treated immune spleen cells

1990 ◽  
Vol 79 (2) ◽  
pp. 246-252 ◽  
Author(s):  
B. RAGER-ZISMAN ◽  
F. ZUCKERMAN ◽  
D. BENHARROCH ◽  
M. PECHT ◽  
Y. BURSTEIN ◽  
...  
Keyword(s):  
Cytomegalovirus Infection ◽  
Humoral Factor ◽  
Murine Cytomegalovirus ◽  
Spleen Cells ◽  
Immune Spleen Cells

Host-Etiological Agent Interactions in Intranasally and Intraperitoneally Induced Cryptococcosis in Mice

1980 ◽  
Vol 29 (2) ◽  
pp. 633-641 ◽  
Author(s):  
Thuang S. Lim ◽  
Juneann W. Murphy ◽  
Larry K. Cauley
Keyword(s):  
Etiological Agent ◽  
Delayed Type Hypersensitivity ◽  
In Vivo Model ◽  
Spleen Cells ◽  
Polysaccharide Antigen ◽  
Cryptococcal Antigen ◽  
Agent Interactions ◽  
Growth Profiles ◽  
Host Parasite

Inbred CBA/J mice were used in developing a defined in vivo model for studying host-parasite relationships in cryptococcosis. Mice were infected either intranasally or intraperitoneally with 10 3 viable Cryptococcus neoformans cells. At weekly intervals over a 92-day period, C. neoformans growth profiles in the lungs, spleens, livers, and brains of the infected animals were determined. In addition, humoral and delayed-type hypersensitivity responses and cryptococcal antigen levels were assayed in these mice. Intranasally infected mice developed strong delayed-type hypersensitivity reactions in response to cryptococcal culture filtrate (CneF) antigen, and there was good correlation between acquisition of delayed-type hypersensitivity and the reduction of C. neoformans cell numbers in infected tissues. In contrast, intraperitoneally infected mice displayed greater numbers of C. neoformans cells in tissues and had somewhat suppressed delayed-type hypersensitivity responses to CneF antigen. Anticryptococcal antibodies were not detected in intranasally or intraperitoneally infected mice, but cryptococcal polysaccharide antigen titers were relatively high in both groups. The transfer of sensitized spleen cells from intranasally infected mice to syngeneic naive recipient mice resulted in the transfer of delayed-type hypersensitivity responsiveness to cryptococcal antigen in the recipients. The intranasally induced infection in mice was similar to the naturally acquired infection in humans; therefore we are proposing that this murine-cryptococcosis model would be useful in gaining a greater understanding of host-etiological agent relationships in this disease.

scholarly journals A reexamination of the role of LYT-2-positive T cells in murine skin graft rejection.

1984 ◽  
Vol 159 (1) ◽  
pp. 57-67 ◽  
Author(s):  
L LeFrancois ◽  
M J Bevan
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Immune Cells ◽  
Graft Rejection ◽  
Skin Grafts ◽  
Complete Elimination ◽  
Spleen Cells ◽  
Relative Contribution ◽  
Immune Spleen Cells

We have investigated which T cell subclass defined by cytolysis with monoclonal anti-Lyt-1.2 and anti-Lyt-2.2 antibodies is required to adoptively transfer the ability to reject skin grafts. B6.Thy-1.1 spleen cells immune to graft antigens were fractionated with antibody plus C' and transferred to adult thymectomized, irradiated, bone marrow-reconstituted (ATXBM) B6.Thy-1.2 hosts that were simultaneously grafted with BALB.B skin. We found that when the ATXBM hosts were used 6 wk after irradiation and marrow reconstitution, both Lyt-1-depleted and Lyt-2-depleted immune spleen cells could transfer the ability to promptly reject skin grafts. However, such ATXBM recipients of Lyt-2-depleted cells that had rejected skin grafts were found to contain graft-specific CTL that were largely of host (B6.Thy-1.2) origin. When ATXBM hosts were used for the experiment 1 wk after irradiation and marrow reconstitution, no host-derived graft-specific CTL could be detected. However, graft rejection occurred in recipients of anti-Lyt-1- or anti-Lyt-2 plus C'-treated immune cells and specific CTL were generated from spleen cells of both groups. Thus, in the absence of a host-derived response, adoptively transferred immune Lyt-2+ cells, either resistant to, or that escaped from, antibody plus C' treatment, are able to expand in response to the antigenic stimulus provided by the graft. A more complete elimination of specific T cell subclasses is therefore needed to assess the relative contribution of a particular subset to the graft rejection process.

scholarly journals The Contributions of Reactive Oxygen Intermediates and Reactive Nitrogen Intermediates to Listericidal Mechanisms Differ in Macrophages Activated Pre- and Postinfection

1998 ◽  
Vol 66 (9) ◽  
pp. 4043-4049 ◽  
Author(s):  
Satoshi Ohya ◽  
Yoshinari Tanabe ◽  
Masato Makino ◽  
Takamasa Nomura ◽  
Huabao Xiong ◽  
...  
Keyword(s):  
Specific Antigen ◽  
Reactive Oxygen ◽  
Reactive Nitrogen ◽  
Reactive Oxygen Intermediates ◽  
Intracellular Killing ◽  
Spleen Cells ◽  
Oxygen Intermediates ◽  
Normal Spleen ◽  
Reactive Nitrogen Intermediates ◽  
Immune Spleen Cells

ABSTRACT The contribution of reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) to the killing of Listeria monocytogenes by macrophages activated by addition of spleen cells from listeria-immune mice plus specific antigen was examined. When macrophages were infected with L. monocytogenes and then spleen cells were added, there was not as big a difference in listericidal activity between macrophages cultured with normal spleen cells and those cultured with immune spleen cells as expected. In this culture system, RNI was mainly involved in the macrophage intracellular killing. In macrophages first activated and then infected, a significant level of enhanced killing was observed. Blockade of ROI production drastically affected the enhanced killing ability, while inhibition of RNI production had a negligible effect. Thus, the contributions of ROI and RNI to listericidal mechanisms of macrophages were different between macrophages activated at pre- and postinfection stages.

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.

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