Induction of T-Helper Cell Activity by Fragments of Rye Grass Pollen Extract Produced by Digestion with Chymotrypsin

1988 ◽  
Vol 87 (4) ◽  
pp. 337-341 ◽  
Author(s):  
R. Standring ◽  
E.A. Lavender ◽  
A.W. Wheeler ◽  
V.M. Spackman ◽  
D.M. Moran
1990 ◽  
Vol 22 ◽  
pp. 53
Author(s):  
M.C. Caroleo ◽  
D. Frasca ◽  
C. Mancini ◽  
G. Nisticò ◽  
G. Doria

1996 ◽  
Vol 26 (3) ◽  
pp. 313-324 ◽  
Author(s):  
Harumi Jyonouchi ◽  
Sining Sun ◽  
Munetaka Mizokami ◽  
Myron D. Gross

1982 ◽  
Vol 155 (3) ◽  
pp. 831-838 ◽  
Author(s):  
J S McDougal ◽  
F W Shen ◽  
S P Cort ◽  
J Bard

The Qa-1 cell surface phenotype reportedly distinguishes two Ly-1 T cell subsets conjointly required for T helper effector activity. Ly-1 cells, obtained from several different priming regimens, were negatively selected with anti-Qa-1 plus complement and compared with unselected Ly-1 cells for helper cell activity. Priming isolated T cells on antigen-pulsed macrophages in the absence of B cells favors the generation of the Ly-1:Qa1- subset, which is capable of efficient helper activity in the absence of the Ly-1:Qa-1+ subset. Priming T cells in an environment containing B cells generates both Ly-1:Qa-1- helper effector cells and Ly-1:Qa-1+ cells which contribute to the helper effect. Whether Ly-1:Qa-1+ cells are capable of independent helper activity cannot be determined, and, as such, Ly-1:Qa-1+ cells are more appropriately termed "help associated" rather than "helper effector." Our results assign a membrane phenotype, Qa-1, which distinguishes an Ly-1 help-associated B cell requiring subset in our system and may prove to be a general marker in a number of systems of Ly-1 inducer cell subsets which functionally require or recognize B cells or their products.


Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1388-1393 ◽  
Author(s):  
EJ Sjamsoedin-Visser ◽  
CJ Heijnen ◽  
BJ Zegers ◽  
JW Stoop

Abstract The capacity of the peripheral blood lymphocytes (PBL) to generate an antibody response in vitro T cell-dependent antigen ovalbumin was studied in 12 severe hemophilia patients who were otherwise in good health. PBL from four of 12 patients were not capable of generating such a response after stimulation in vitro, whereas all controls were normal. This negative plaque-forming cell (PFC) response coincided with the presence of antibodies directed toward human T-lymphotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV). Only one patient with antibodies against HTLV-III/LAV had a normal PFC response. The negative PFC response was not due to a deficient T helper cell activity, nor to an excessive T suppressor cell function. However, in the peripheral blood of these four patients, the presence of activated B cells that are refractory to antigen-specific T helper cell signals and secrete specific antibodies spontaneously could be demonstrated. Most of the patients showed a hyperimmunoglobulinemia. No correlation between the T4/T8 ratio and the level of the PFC response was demonstrable. From the data obtained in these investigations we raise the hypothesis that infection with HTLV-III/LAV in hemophilia patients will lead to in vivo (pre)activation of B cells that results in unresponsiveness or decreased response to antigen-specific signals.


Immunology ◽  
2010 ◽  
Vol 131 (4) ◽  
pp. 488-500 ◽  
Author(s):  
Thomas Bollinger ◽  
Annalena Bollinger ◽  
Julius Naujoks ◽  
Tanja Lange ◽  
Werner Solbach

1983 ◽  
Vol 409 (1 The Secretory) ◽  
pp. 230-237 ◽  
Author(s):  
C. O. Elson ◽  
D. B. Weiserbs ◽  
W. Ealding ◽  
E. Machelski

2021 ◽  
Vol 12 ◽  
Author(s):  
Derek Tobin ◽  
Runar Vige ◽  
Philip C. Calder

Over the last 15 years there has been an accumulation of data supporting the concept of a gut-brain axis whereby dysbiosis of the gut microbiota can impact neurological function. Such dysbiosis has been suggested as a possible environmental exposure triggering multiple sclerosis (MS). Dysbiosis has been consistently shown to result in a reduction in short-chain fatty acid (SCFA) producing bacteria and a reduction in stool and plasma levels of propionate has been shown for MS patients independent of disease stage and in different geographies. A wealth of evidence supports the action of propionate on T-cell activity, resulting in decreased T-helper cell 1 (Th1) and T-helper cell 17 (Th17) numbers/activity and increased regulatory T cell (Treg cell) numbers/activity and an overall anti-inflammatory profile. These different T-cell populations play various roles in the pathophysiology of MS. A recent clinical study in MS patients demonstrated that supplementation of propionate reduces the annual relapse rate and slows disease progression. This review discusses this data and the relevant mechanistic background and discusses whether taming of the overactive immune system in MS is likely to allow easier bacterial and viral infection.


2016 ◽  
Vol 245 ◽  
pp. 52-58 ◽  
Author(s):  
Cindy Strehl ◽  
Saskia Schellmann ◽  
Lionel Maurizi ◽  
Margarethe Hofmann-Amtenbrink ◽  
Thomas Häupl ◽  
...  

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