Speculation on the Use of Adoptive Immunity in Malarial Vaccination

2015 ◽  
pp. 94-96
Author(s):  
Charles L. Greenblatt ◽  
Raymond L. Jacobson
Keyword(s):  
Adoptive Immunity

scholarly journals T cell suppressors of antitumor immunity. The production of Ly-1-,2+ suppressors of delayed sensitivity precedes the production of suppressors of protective immunity.

1986 ◽  
Vol 164 (4) ◽  
pp. 1179-1192 ◽  
Author(s):  
A DiGiacomo ◽  
R J North
Keyword(s):  
T Cell ◽  
Tumor Growth ◽  
Antitumor Immunity ◽  
Tumor Antigens ◽  
Suppressor Cell ◽  
Passive Transfer ◽  
Concomitant Immunity ◽  
Adoptive Immunity ◽  
Suppressor T Lymphocytes ◽  
Early Tumor

The results of this study show that during growth of the immunogenic Meth A fibrosarcoma, two different types of suppressor T lymphocytes are generated in sequence. One type is generated during early tumor growth, reaches peak number around day 6, and is progressively lost thereafter. It is defined by its ability, upon passive transfer, to suppress the expression of a DTH reaction to tumor antigens in tumor-immunized recipients. It bears the Ly1-,2+ membrane phenotype and is sensitive to relatively low doses of cyclophosphamide. In contrast, the second type of suppressor cell is not detected until after day 9 of tumor growth, and is defined by its ability to inhibit, upon passive transfer, the expression of adoptive immunity against an established tumor in T cell-deficient recipients. According to previous studies it bears the Ly1+,2-, L3T4a+ membrane phenotype and is less sensitive to cyclophosphamide than the T cell suppressor of DTH. It is argued that this second type of suppressor T cell seems likely to be responsible for the escape of immunogenic tumors from antitumor immunity, because it can suppress the expression of a powerful mechanism of antitumor immunity in recipient mice, and is generated progressively as the tumor-bearing host loses concomitant immunity. In contrast, although the Ly-1-,2+ T cell suppressors of DTH can efficiently suppress a DTH reaction to an implant of living tumor cells, they fail to suppress the expression of immunity to the same implant.

scholarly journals Management of celiac disease: from evidence to clinical practice

2017 ◽  
Vol 11 (4) ◽  
pp. 345
Author(s):  
Tiziana M. Attardo ◽  
Elena Magnani ◽  
Carlotta Casati ◽  
Danilo Cavalieri ◽  
Pietro Crispino ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Diagnostic Tests ◽  
Genetic Factors ◽  
Clinical Presentation ◽  
Scientific Evidence ◽  
Methodological Approach ◽  
Human Leukocyte ◽  
Gluten Sensitivity ◽  
Adoptive Immunity

Celiac disease (CD) is a complex polygenic disorder, which involves genetic factors human leukocyte complex (HLA) and non-HLA genes, environmental factors, innate and adoptive immunity, and a robust chronic T-mediated autoimmune component. The main goal of the present monograph is to define a methodological approach for the disease, characterized by frequent late diagnosis, in order for the physician to become aware of the disease management, the diversity of the clinical presentation itself and in different patients. A unique attention is payed to the specific diagnostic tests to define a correct and accurate application of them, and in addition, to disease follow-up and possible complications. Moreover, a dedicated space is assigned to refractory CD, to potential CD and non-celiac gluten sensitivity. Legislative aspects of the celiac disease in Italy are addressed, too. The celiac disease guidelines and their evaluation by means of Appraisal of Guidelines, Research and Evaluation II instrument allow us to classify the different recommendations and to apply them according to the stakeholders’ involvement, pertinence, methodological accuracy, clarity and publishing independence. Finally, the most current scientific evidence is taken into account to create a complete updated monograph.

scholarly journals Expression of passively transferred immunity against an established tumor depends on generation of cytolytic T cells in recipient. Inhibition by suppressor T cells.

1983 ◽  
Vol 157 (5) ◽  
pp. 1448-1460 ◽  
Author(s):  
C D Mills ◽  
R J North
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Cell ◽  
Cell Response ◽  
Passive Transfer ◽  
T Cell Response ◽  
Suppressor T Cells ◽  
Tumor Bearing ◽  
Draining Lymph Node ◽  
Adoptive Immunity

The results of this study with the P815 mastocytoma confirm the results of previous studies that showed that the passive transfer of tumor-sensitized T cells from immunized donors can cause the regression of tumors growing in T cell-deficient (TXB) recipients, but not in normal recipients. The key additional finding was that the expression of adoptive immunity against tumors growing in TXB recipients is immediately preceded by a substantial production of cytolytic T cells in the recipients' draining lymph node. On the other hand, failure of adoptive immunity to be expressed against tumors growing in normal recipients was associated with a cytolytic T cell response of much lower magnitude, and a similar low magnitude response was generated in TXB recipients infused with normal spleen cells and in tumor-bearing control mice. Because the passively transferred sensitized T cells possessed no cytolytic activity of their own, the results indicate that the 6-8-d delay before adoptive immunity is expressed represents the time needed for passively transferred helper or memory T cells to give rise to a cytolytic T cell response of sufficient magnitude to destroy the recipient's tumor. In support of this interpretation was the additional finding that inhibition of the expression of adoptive immunity by the passive transfer of suppressor T cells from tumor-bearing donors was associated with a substantially reduced cytolytic T cell response in the recipient's draining lymph node. The results serve to illustrate that interpretation of the results of adoptive immunization experiments requires a knowledge of the events that take place in the adoptively immunized recipient. They support the interpretation that suppressor T cells function in this model to "down-regulate" the production of cytolytic effector T cells.

scholarly journals Kunkel Lecture: Fundamental immunodeficiency and its correction

2017 ◽  
Vol 214 (8) ◽  
pp. 2175-2191 ◽  
Author(s):  
Carl Nathan
Keyword(s):  
Immune System ◽  
Antimicrobial Agents ◽  
Host Immunity ◽  
Host Gene ◽  
Primary Immunodeficiencies ◽  
Human Species ◽  
Adoptive Immunity ◽  
Healthy Host

“Fundamental immunodeficiency” is the inability of the encoded immune system to protect an otherwise healthy host from every infection that could threaten its life. In contrast to primary immunodeficiencies, fundamental immunodeficiency is not rare but nearly universal. It results not from variation in a given host gene but from the rate and extent of variation in the genes of other organisms. The remedy for fundamental immunodeficiency is “adopted immunity,” not to be confused with adaptive or adoptive immunity. Adopted immunity arises from four critical societal contributions to the survival of the human species: sanitation, nutrition, vaccines, and antimicrobial agents. Immunologists have a great deal to contribute to the development of vaccines and antimicrobial agents, but they have focused chiefly on vaccines, and vaccinology is thriving. In contrast, the effect of antimicrobial agents in adopted immunity, although fundamental, is fragile and failing. Immunologists can aid the development of sorely needed antimicrobial agents, and the study of antimicrobial agents can help immunologists discover targets and mechanisms of host immunity.

Transfer of adoptive immunity by intra-arterial injection of tumor-immune pig lymph node cells

Urology ◽  
1978 ◽  
Vol 12 (4) ◽  
pp. 398-401 ◽  
Author(s):  
M.O. Symes ◽  
J.P. Mitchell ◽  
H. Eckert ◽  
J.B.M. Roberts ◽  
R.C.L. Feneley ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Node Cells ◽  
Adoptive Immunity
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