scholarly journals INITIATION OF ANTIBODY RESPONSES BY DIFFERENT CLASSES OF LYMPHOCYTES

1969 ◽  
Vol 130 (4) ◽  
pp. 895-906 ◽  
Author(s):  
Samuel Strober
Keyword(s):  
Antibody Response ◽  
Thoracic Duct ◽  
Salmonella Typhi ◽  
Primary Response ◽  
Primary Antibody ◽  
Spleen Cells ◽  
Normal Cells ◽  
Duct Cells ◽  
Primary Antibody Response

Thoracic duct cells and spleen cells were tested for their ability to restore the primary antibody response of X-irradiated rats to bovine serum albumin (BSA), sheep red blood cells (SRBC), horse spleen femtin (HSF), and Salmonella typhi flagella. Spleen cells were at least as efficient as thoracic duct cells in restoring the response to BSA, HSF, and Salmonella typhi flagella. In further experiments thoracic duct cells lacking large dividing lymphocytes were tested for their ability to restore the primary response. Large lymphocytes were eliminated by the in vitro incubation of thoracic duct cells for 24 hr at 37°C or by treatment of thoracic duct cell donors with the mitotic inhibitor vinblastine sulfate 24 hr prior to cannulation of the thoracic duct. Experiments with SRBC show that incubated cells and cells from vinblastine-treated donors are as efficient as normal cells in restoring the primary antibody response. On the other hand, experiments with HSF and Salmonella typhi flagella show that incubated cells and cells from vinblastine-treated donors are about five times less efficient than normal cells in restoring the response. Normal thoracic duct cells were more efficient than incubated cells but less efficient than cells from vinblastine-treated donors in restoring the early response to BSA. The experimental findings indicate that the classes of thoracic duct lymphocytes which initiate the primary antibody response to SRBC differ from the classes which initiate the response to HSF and Salmonella typhi flagella, or BSA.

scholarly journals IN VITRO INDUCTION OF A PRIMARY RESPONSE TO THE DINITROPHENYL DETERMINANT

1970 ◽  
Vol 131 (1) ◽  
pp. 93-99 ◽  
Author(s):  
Shraga Segal ◽  
Amiela Globerson ◽  
Michael Feldman ◽  
Joseph Haimovich ◽  
Michael Sela
Keyword(s):  
Antibody Response ◽  
Normal Mouse ◽  
Culture Medium ◽  
Primary Response ◽  
Primary Antibody ◽  
Primary Antibody Response ◽  
T4 Phage ◽  
In Vitro Induction ◽  
Stimulation Of

Primary antibody response against the dinitrophenyl group has been elicited in vitro after the stimulation of normal mouse spleen explants with 2,4-dinitrophenyl (DNP)-hemocyanin or α-DNP-poly-L-lysine (PLL). Antibodies were detected in the culture medium by the inactivation of DNP-T4 phage. The specificity of the reaction was manifested by the lack of the capacity of the medium to inactivate the unmodified bacteriophage and by the inhibition of the inactivation of DNP-T4 with DNP-lysine.

Primary Antibody Response by Chicken Spleen Cells In Vitro

1974 ◽  
Vol 3 (5) ◽  
pp. 589-596
Author(s):  
G. TUFVESON ◽  
I. LUNDBERG ◽  
G V ALM
Keyword(s):  
Antibody Response ◽  
Primary Antibody ◽  
Spleen Cells ◽  
Chicken Spleen ◽  
Primary Antibody Response

scholarly journals HOMEOSTASIS OF ANTIBODY FORMATION IN THE ADULT RAT

1964 ◽  
Vol 120 (6) ◽  
pp. 987-1005 ◽  
Author(s):  
Donald A. Rowley ◽  
Frank W. Fitch
Keyword(s):  
Antibody Response ◽  
Specific Antibody ◽  
Antibody Formation ◽  
Sheep Erythrocyte ◽  
Passive Immunization ◽  
Primary Antibody ◽  
Secondary Response ◽  
Primary Antibody Response

Passive immunization of rats with homologous anti-sheep erythrocyte serum markedly inhibited the primary antibody response to various doses of sheep erythrocytes. Inhibition was "specific" and apparently produced by either "19S" or "7S" antibody to the antigen. Passive immunization inhibited splenic hyperplasia associated with the primary antibody response. Passive immunization 24 hours after active immunization effectively inhibited the primary antibody response. The markedly suppressive effect of specific antibody on the primary antibody response contrasted sharply with the absence of this effect on the secondary response. Antigen-antibody complexes formed in vitro elicited no measurable primary antibody response but did elicit a high secondary response. Exposure of normal spleen cells to the antibody in vivo or in vitro suppressed their response to the antigen in x-irradiated recipients. In contrast, cells from previously immunized animals transferred to x-irradiated animals produced antibody in the presence of passively given antibody. Thus, "potential antibody-forming cells" from normal animals were unresponsive to the antigen in the presence of specific antibody, while "antibody-forming cells" from previously immunized animals responded to the antigen in the presence of antibody. Presumably, antibody actively produced in small quantities by a few antibody-forming cells might inhibit antibody formation by potential antibody-forming cells. Confirmation of this suggestion was obtained by showing that some animals initially injected with small doses of antigen failed to produce measurable antibody to subsequent injections of larger doses of the antigen. Low doses of antigen capable of inducing unresponsiveness produced no measurable circulating antibody, but these doses did produce increased numbers of plaque-forming (antibody-releasing) cells in spleens of rats. Thus, the formation of specific antibody may provide a homeostatic or "feed-back" mechanism which controls or limits production of specific antibody to the portion of the antibody-forming system previously stimulated by the antigen. This mechanism may account in part for immunological unresponsiveness produced in certain other related experimental systems.

Physiological and supraphysiological supplements of triiodothyronine do not influence the primary in vitro antibody response to trinitrophenylated Brucella abortus by spleen cells in serum-containing media

1988 ◽  
Vol 118 (3) ◽  
pp. 351-356 ◽  
Author(s):  
S.M. Filteau ◽  
Bill Woodward
Keyword(s):  
Antibody Response ◽  
Brucella Abortus ◽  
Plasma Cells ◽  
Immune Reaction ◽  
Antibody Responses ◽  
Spleen Cells ◽  
Accessory Cells ◽  
Primary Antibody Response

Abstract. T3 supplements enhance splenic primary thymus-independent antibody responses in the mouse in vivo. The purpose of the present investigation was to determine whether this effect may be mediated, in part, by direct influences on the lymphocytes and/or accessory cells involved in the response. A range of T3 levels (3 × 10−10 to 10−5 mol/l) was tested in microcultures of separated spleen cells from CBA/J mice 33 days of age. The immune reaction examined in vitro was the primary antibody response to trinitrophenylated Brucella abortus (TNP-BA). T3 was without influence, throughout the concentration range tested, on the number of anti-TNP plasma cells generated per culture. This result was obtained using splenocytes either from well-nourished or from malnourished mice, and using both optimal and suboptimal numbers of TNP-BA. On the basis of the present results and a reinterpretation of previous published work, it is concluded that the influence of T3 supplements on splenic antibody responses in vivo is mediated indirectly. Direct influences of T3 on the T-independent antibody response, if such occur, must be maximized by subphysiological levels of the hormone.

scholarly journals Antigen acquisition by dendritic cells: intestinal dendritic cells acquire antigen administered orally and can prime naive T cells in vivo.

1993 ◽  
Vol 177 (5) ◽  
pp. 1299-1307 ◽  
Author(s):  
L M Liu ◽  
G G MacPherson
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Antibody Response ◽  
Thoracic Duct ◽  
Oral Feeding ◽  
Thoracic Duct Lymph ◽  
Duct Lymph ◽  
Primary Antibody Response

In the rat, mesenteric lymphadenectomy allows collection of dendritic cells (DC) derived from the small intestine after cannulation of the thoracic duct. We prepared rats this way and administered antigens by oral feeding or intraintestinal injection. DC enriched from the thoracic duct lymph collected over the first 24 h from these animals are able to stimulate sensitized T cells in vitro and to prime popliteal lymph node CD4+ T cells after footpad injection, while B and T cells from the same thoracic duct lymph are inert in priming. 500 or less DC pulsed in vitro with antigen can prime T cells in vivo, whereas 100 times more B cells or macrophages pulsed in vitro are quite inert. 1 mg of ovalbumin administered orally is sufficient to load DC for in vivo priming of T cells. Antigen could not be detected directly in DC but was present in macrophages in the lamina propria. Direct presentation of antigen by DC to T cells was demonstrated by injecting F1 recipients with parental DC and showing restriction of T cell sensitization to the major histocompatibility complex of the injected DC. Antigen-bearing DC do not induce a detectable primary antibody response but a small secondary antibody response can be detected after a boosting injection. These results show that acquisition of antigens by DC in the intestine is very similar to what occurs in vitro or in other tissues, suggesting that there may be no special difference in antigen handling at mucosal surfaces. One implication of these results is that hypotheses designed to explain oral tolerance must take into account the presence of immunostimulatory, antigen-bearing DC in animals that have received oral antigens.

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