Cellular Immune Response to Viruses and the Biological Role of Polymorphic Major Transplantation Antigens

1979 ◽  
pp. 171-204 ◽  
Author(s):  
R. M. Zinkernagel
2019 ◽  
Vol 20 (2) ◽  
pp. 271 ◽  
Author(s):  
Przemyslaw Zdziarski

Although the existing paradigm states that cytomegalovirus (CMV) reactivation is under the control of the cellular immune response, the role of humoral and innate counterparts are underestimated. The study analyzed the host–virus interaction i.e., CMV-immune response evolution during infection in three different clinical situations: (1) immunodeficient CMV-positive human leukocyte antigen (HLA)-matched bone marrow recipients after immunoablative conditioning as well as immunocompetent, (2) adult, and (3) infant with primary immune response. In the first situation, a fast and significant decrease of specific immunity was observed but reconstitution of marrow-derived B and natural killer (NK) cells was observed prior to thymic origin of T cells. The lowest CMV-IgG (93.2 RU/mL) was found just before CMV viremia. It is noteworthy that the sole and exclusive factor of CMV-specific immune response is a residual recipient antibody class IgG. The CMV-quantiferon increase was detected later, but in the first phase, phytohemagglutinin (PHA)-induced IFN-γ release was significantly lower than that of CMV-induced (“indeterminate” results). It corresponds with the increase of NK cells at the top of lymphocyte reconstitution and undetected CMV-specific CD8 cells using a pentamer technique. In immunocompetent adult (CMV-negative donor), the cellular and humoral immune response increased in a parallel manner, but symptoms of CMV mononucleosis persisted until the increase of specific IgG. During infancy, the decrease of the maternal CMV-IgG level to 89.08 RU/mL followed by clinical sequel, i.e., CMV replication, were described. My observations shed light on a unique host-CMV interaction and CMV-IgG role: they indicate that its significant decrease predicts CMV replication. Before primary cellular immune response development, the high level of residual CMV-IgG (about >100 R/mL) from mother or recipient prevents virus reactivation. The innate immune response and NK-dependent IFN-secretion should be further investigated.


2006 ◽  
Vol 52 (7) ◽  
pp. 711-716 ◽  
Author(s):  
Marcela B. Figueiredo ◽  
Daniele P. Castro ◽  
Nadir F. S. Nogueira ◽  
Eloi S. Garcia ◽  
Patrícia Azambuja

2004 ◽  
Vol 25 (6) ◽  
pp. 401-406 ◽  
Author(s):  
İrfan Kaygusuz ◽  
Ahmet Gödekmerdan ◽  
Erol Keleş ◽  
Turgut Karlidağ ◽  
Sinasi Yalçin ◽  
...  

1996 ◽  
Vol 11 (3) ◽  
pp. 474-480 ◽  
Author(s):  
C. Tzanno-Martins ◽  
L. S. Azevedo ◽  
N. Orii ◽  
E. Futata ◽  
V. Jorgetti ◽  
...  

PEDIATRICS ◽  
1975 ◽  
Vol 56 (4) ◽  
pp. 498-500
Author(s):  
Gary S. Rachelefsky ◽  
E. Richard Stiehm

A new clue in the quest for an etiology of the rheumatic diseases may be the newfound association of certain of these disorders with the presence of the genetically inherited histocompatibility antigen, HL-A W27. The frequency of this antigen is 5% to 10% in the general population; by contrast, its frequency is 85% to 90% in adults with ankylosing spondylitis and Reiter's syndrome and 35% to 40% in children with juvenile rheumatoid arthritis. Histocompatibility transplantation antigens are present on the surface of most cells (not erythrocytes) which are capable of inducing a cellular immune response in another of the same species and result in rejection of transplanted tissue or cells.


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