The Hereditary Human Gamma Globulin (Gm) Groups and the Structural Subunits of Human ?-Globulin

2015 ◽  
pp. 483-490 ◽  
Author(s):  
H. H. Fudenberg ◽  
E. C. Franklin
Keyword(s):  
Gamma Globulin ◽  
Human Gamma Globulin

scholarly journals Antibody Prophylaxis and Therapy against West NileVirus Infection in Wild-Type and ImmunodeficientMice

2003 ◽  
Vol 77 (24) ◽  
pp. 12941-12949 ◽  
Author(s):  
Michael J. Engle ◽  
Michael S. Diamond
Keyword(s):  
B Cell ◽  
Gamma Globulin ◽  
Polyclonal Antibodies ◽  
Current Treatment ◽  
Mouse Serum ◽  
Wild Type ◽  
Viral Reservoirs ◽  
In The Wild ◽  
Human Gamma Globulin ◽  
Immune Antibody

ABSTRACT West Nile virus (WNV) is a mosquito-borne Flavivirus that causes encephalitis in a subset of susceptible humans. Current treatment for WNV infections is supportive, and no specific therapy or vaccine is available. In this study, we directly tested the prophylactic and therapeutic efficacy of polyclonal antibodies against WNV. Passive administration of human gamma globulin or mouse serum prior to WNV infection protected congenic wild-type, B-cell-deficient (μMT), and T- and B-cell-deficient (RAG1) C57BL/6J mice. Notably, no increased mortality due to immune enhancement was observed. Although immune antibody completely prevented morbidity and mortality in wild-type mice, its effect was not durable in immunocompromised mice: many μMT and RAG1 mice eventually succumbed to infection. Thus, antibody by itself did not completely eliminate viral reservoirs in host tissues, consistent with an intact cellular immune response being required for viral clearance. In therapeutic postexposure studies, human gamma globulin partially protected against WNV-induced mortality. In μMT mice, therapy had to be initiated within 2 days of infection to gain a survival benefit, whereas in the wild-type mice, therapy even 5 days after infection reduced mortality. This time point is significant because between days 4 and 5, WNV was detected in the brains of infected mice. Thus, passive transfer of immune antibody improves clinical outcome even after WNV has disseminated into the central nervous system.

Prevention of paralytic poliomyelitis in tonsillectomized cynomolgus monkeys by human gamma globulin

1953 ◽  
Vol 15 (3) ◽  
pp. 408-409
Author(s):  
J.M. Adams ◽  
R.A. Boak ◽  
C.M. Carpenter ◽  
J.D. French ◽  
S.J. Klein ◽  
...  
Keyword(s):  
Gamma Globulin ◽  
Paralytic Poliomyelitis ◽  
Cynomolgus Monkeys ◽  
Human Gamma Globulin

scholarly journals THE ABILITY OF BACTERIAL LIPOPOLYSACCHARIDE TO MODULATE THE INDUCTION OF UNRESPONSIVENESS TO A STATE OF IMMUNITY

1973 ◽  
Vol 138 (6) ◽  
pp. 1481-1495 ◽  
Author(s):  
J. A. Louis ◽  
J. M. Chiller ◽  
W. O. Weigle
Keyword(s):  
T Cell ◽  
Temporal Relationship ◽  
Gamma Globulin ◽  
Bacterial Lipopolysaccharide ◽  
Secondary Response ◽  
Transfer System ◽  
Primary Antibody Response ◽  
Human Gamma Globulin ◽  
Cell Cooperation ◽  
Induction Of Tolerance

Studies were performed to define the cellular parameters involved in the interference with the induction of immunologic unresponsiveness to human gamma globulin (HGG) by bacterial lipopolysaccharide (LPS). Mice which were injected with deaggregated HGG (tolerogen) and with LPS did not become tolerant to that antigen, but rather became primed to a subsequent challenge with immunogen. The ability to prime with tolerogen and LPS was also demonstrated in an adoptive transfer system. The temporal relationship between the injection of tolerogen and that of LPS was critical for priming to occur. The injection of tolerogen and LPS not only primed mice to HGG, but also resulted in a primary antibody response to HGG. The capacity of LPS to interfere with the induction of tolerance was restricted to B cells and did not affect the ability to induce unresponsiveness in T cells. The secondary response to HGG in mice primed by tolerogen and LPS was found to be T-cell independent. These observations are interpreted and discussed from the standpoint of the ability of LPS to circumvent required T-cell cooperation and to modulate to tolerogenic stimulus into an immunogenic signal.

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