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.

scholarly journals Terminal Deoxynucleotidyl Transferase Is Not Required for Antibody Response to Polysaccharide Vaccines againstStreptococcus pneumoniaeandSalmonella entericaSerovar Typhi

2018 ◽  
Vol 86 (9) ◽  
Author(s):  
Vivek Belde ◽  
Matthew P. Cravens ◽  
Dania Gulandijany ◽  
Justin A. Walker ◽  
Isabel Palomo-Caturla ◽  
...  
Keyword(s):  
Antibody Response ◽  
B Cell ◽  
Salmonella Enterica ◽  
Passive Immunization ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Human Infants ◽  
Content Type ◽  
Serovar Typhimurium

ABSTRACTB cell antigen receptor (BCR) diversity increases by several orders of magnitude due to the action of terminal deoxynucleotidyl transferase (TdT) during V(D)J recombination. Unlike adults, infants have limited BCR diversity, in part due to reduced expression of TdT. Since human infants and young mice respond poorly to polysaccharide vaccines, such as the pneumococcal polysaccharide vaccine Pneumovax23 and Vi polysaccharide (ViPS) ofSalmonella entericaserovar Typhi, we tested the contribution of TdT-mediated BCR diversity in response to these vaccines. We found that TdT+/−and TdT−/−mice generated comparable antibody responses to Pneumovax23 and survivedStreptococcus pneumoniaechallenge. Moreover, passive immunization of B cell-deficient mice with serum from Pneumovax23-immunized TdT+/−or TdT−/−mice conferred protection. TdT+/−and TdT−/−mice generated comparable levels of anti-ViPS antibodies and antibody-dependent, complement-mediated bactericidal activity againstS. Typhiin vitro. To test the protective immunity conferred by ViPS immunizationin vivo, TdT+/−and TdT−/−mice were challenged with a chimericSalmonella entericaserovar Typhimurium strain expressing ViPS, since mice are nonpermissive hosts forS. Typhi infection. Compared to their unimmunized counterparts, immunized TdT+/−and TdT−/−mice challenged with ViPS-expressingS. Typhimurium exhibited a significant reduction in the bacterial burden and liver pathology. These data suggest that the impaired antibody response to the Pneumovax23 and ViPS vaccines in the young is not due to limited TdT-mediated BCR diversification.

scholarly journals THE EFFECT OF AMINOMETHYLPTEROYLGLUTAMIC ACID ON THE DEVELOPMENT OF SKIN HYPERSENSITIVITY AND ON ANTIBODY FORMATION IN GUINEA PIGS

1961 ◽  
Vol 114 (2) ◽  
pp. 173-183 ◽  
Author(s):  
Robert M. Friedman ◽  
Charles E. Buckler ◽  
Samuel Baron
Keyword(s):  
Antibody Response ◽  
Guinea Pigs ◽  
Antibody Formation ◽  
Diphtheria Toxoid ◽  
Primary Antibody ◽  
Febrile Response ◽  
Skin Hypersensitivity ◽  
Antigenic Stimulus ◽  
Primary Antibody Response

1. In guinea pigs, aminomethylpteroylglutamic acid (methotrexate) is capable of blocking the development of delayed skin hypersensitivity, the primary antibody response, and the specific febrile response to ovalbumin and diphtheria toxoid. The primary antibody response is more easily inhibited than is the development of delayed skin hypersensitivity. 2. The effect of methotrexate on immunologic responses depended upon the dose of methotrexate employed and the strength of the antigenic stimulus.

scholarly journals THE X-Y-Z SCHEME OF IMMUNOCYTE MATURATION

1968 ◽  
Vol 128 (4) ◽  
pp. 715-728 ◽  
Author(s):  
Vera S. Byers ◽  
Eli E. Sercarz
Keyword(s):  
Bovine Serum Albumin ◽  
Antibody Response ◽  
Serum Albumin ◽  
Lymph Nodes ◽  
Bovine Serum ◽  
Antibody Formation ◽  
Memory Cell ◽  
Secondary Response ◽  
Antigen Concentration

A concentration of 5 mg/ml bovine serum albumin (BSA) prevents the in vitro elicitation of a secondary response in primed rabbit popliteal lymph nodes, if it is left in contact with the node fragments for the first 6 days of culture. No antibody formation can be detected at any time during the culture period in most cases, although occasional fragments are resistant to inhibition. Reducing the exposure time to the first 3 days of culture delays the peak of the antibody response. The inhibition is antigen specific. Reconstruction experiments demonstrate that the inhibition is not due to antigen masking of the antibody. Even shortly after optimal stimulation, the addition of 5 mg/ml BSA to the fragments was not able to prevent a normal antibody response. The implications of these findings are that (a) a high antigen concentration suspends the memory cell in a reversibly paralyzed state, (b) memory cells have a heterogeneous susceptibility to inhibition, (c) once induced, the antibody response cannot be inhibited by antigen overloading, (d) unresponsiveness in a primed animal can be due to either exhaustion of the memory cell population or paralysis of the memory cell.

scholarly journals The Immune Enhancement of Sodium Lauryl Sulfoacetate in Chickens

2010 ◽  
Vol 2010 ◽  
pp. 1-5
Author(s):  
DaRong Cheng ◽  
ShanYuan Zhu ◽  
HuaiChang Sun
Keyword(s):  
T Cell ◽  
Antibody Response ◽  
Specific Antibody ◽  
Mononuclear Cells ◽  
Control Group ◽  
Peripheral Blood Mononuclear ◽  
Specific Antibody Response ◽  
Cell Ratio

The purpose of this study is to investigate feasibility of sodium lauryl sulfoacetate (SLS) as an immunoadjuvant in chickens. After treating with 62.5, 125, 250, or 500 μg/mL SLS in vitro, lymphocyte proliferation assay of chicken peripheral blood mononuclear cells showed that theOD570values of all experimental groups, as well as Con A-stimulated group, were significantly higher than that of the untreated control group. After injection with 1.0, 2.0, or 4.0 mg/kg of SLS for 3 consecutive days, chickens were vaccinated with an attenuated vaccine againstNewcastle disease virus(NDV), and the immunoadjuvant effects of SLS were evaluated on the basis of immune organ index, antibody response, andCD4+/CD8+T-cell ratio. The results confirmed that SLS could enhance NDV-specific antibody response and increaseCD4+/CD8+T-cell ratio in vivo. Furthermore, SLS could improve NDV-specific antibody response in thiamphenicol-treated chickens. These data indicate that SLS not only can improve humoral immune response but also reverse the immunosuppressive effect of thiamphenicol in chickens.

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.

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