scholarly journals Review: The Nutritional Management of Multiple Sclerosis With Propionate

2021 ◽  
Vol 12 ◽  
Author(s):  
Derek Tobin ◽  
Runar Vige ◽  
Philip C. Calder
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
Cell Activity ◽  
T Helper Cell ◽  
Disease Stage ◽  
Helper Cell ◽  
T Helper ◽  
Annual Relapse Rate ◽  
Recent Clinical Study ◽  
Inflammatory Profile

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.

Fewer protective cytotoxic T-cell epitopes than T-helper-cell epitopes on vesicular stomatitis virus.

1993 ◽  
Vol 67 (6) ◽  
pp. 3680-3683 ◽  
Author(s):  
T M Kündig ◽  
I Castelmur ◽  
M F Bachmann ◽  
D Abraham ◽  
D Binder ◽  
...  
Keyword(s):  
T Cell ◽  
Vesicular Stomatitis Virus ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cytotoxic T Cell ◽  
T Cell Epitopes ◽  
T Helper ◽  
Vesicular Stomatitis

scholarly journals T helper cell type 1 (Th1), Th2 and Th17 responses to myelin basic protein and disease activity in multiple sclerosis

Immunology ◽  
2008 ◽  
Vol 125 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Chris J. Hedegaard ◽  
Martin Krakauer ◽  
Klaus Bendtzen ◽  
Henrik Lund ◽  
Finn Sellebjerg ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Activity ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type

Mls AND THE HELPER T-CELL REPERTOIRE I. Mls as a regulator of T-helper cell activation

1988 ◽  
Vol 15 (1-3) ◽  
pp. 169-174 ◽  
Author(s):  
U. Hämmerling ◽  
M. Toulon ◽  
R. G. E. Palfree ◽  
M. K. Hoffmann
Keyword(s):  
T Cell ◽  
Cell Activation ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Cell Repertoire ◽  
T Helper ◽  
Helper T Cell ◽  
Cell Repertoire

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
Keyword(s):  
Grass Pollen ◽  
Cell Activity ◽  
T Helper Cell ◽  
Helper Cell ◽  
Pollen Extract ◽  
T Helper ◽  
Rye Grass

scholarly journals Regulation of T Cell Responses by Ionic Salt Signals

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2365
Author(s):  
Christina E. Zielinski
Keyword(s):  
T Cells ◽  
T Cell ◽  
Sodium Chloride ◽  
T Cell Responses ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Tissue Microenvironment ◽  
Cell Responses ◽  
The Impact

T helper cell responses are tailored to their respective antigens and adapted to their specific tissue microenvironment. While a great proportion of T cells acquire a resident identity, a significant proportion of T cells continue circulating, thus encountering changing microenvironmental signals during immune surveillance. One signal, which has previously been largely overlooked, is sodium chloride. It has been proposed to have potent effects on T cell responses in the context of autoimmune, allergic and infectious tissue inflammation in mouse models and humans. Sodium chloride is stringently regulated in the blood by the kidneys but displays differential deposition patterns in peripheral tissues. Sodium chloride accumulation might furthermore be regulated by dietary intake and thus by intentional behavior. Together, these results make sodium chloride an interesting but still controversial signal for immune modulation. Its downstream cellular activities represent a potential therapeutic target given its effects on T cell cytokine production. In this review article, we provide an overview and critical evaluation of the impact of this ionic signal on T helper cell polarization and T helper cell effector functions. In addition, the impact of sodium chloride from the tissue microenvironment is assessed for human health and disease and for its therapeutic potential.

scholarly journals Autopathogenic T Helper Cell Type 1 (Th1) and Protective Th2 Clones Differ in Their Recognition of the Autoantigenic Peptide of Myelin Proteolipid Protein

1997 ◽  
Vol 186 (6) ◽  
pp. 867-876 ◽  
Author(s):  
Mercy Prabhu Das ◽  
Lindsay B. Nicholson ◽  
Judith M. Greer ◽  
Vijay K. Kuchroo
Keyword(s):  
T Cell ◽  
Proteolipid Protein ◽  
T Helper Cell ◽  
Autoimmune Response ◽  
Helper Cell ◽  
Th2 Cells ◽  
T Helper ◽  
Myelin Proteolipid Protein ◽  
Contact Residue ◽  
Myelin Proteolipid

We previously generated a panel of T helper cell 1 (Th1) clones specific for an encephalitogenic peptide of myelin proteolipid protein (PLP) peptide 139–151 (HSLGKWLGHPDKF) that induces experimental autoimmune encephalomyelitis (EAE) upon adoptive transfer. In spite of the differences in their T cell receptor (TCR) gene usage, all these Th1 clones required W144 as the primary and most critical TCR contact residue for the activation. In this study, we determined the TCR contact residues of a panel of Th2/Th0 clones specific for the PLP peptide 139–151 generated either by immunization with the PLP 139–151 peptide with anti– B7-1 antibody or by immunization with an altered peptide Q144. Using alanine-substituted peptide analogues of the native PLP peptide, we show that the Th2 clones have shifted their primary contact residue to the NH2-terminal end of the peptide. These Th2 cells do not show any dependence on the W144, but show a critical requirement for L141/G142 as their major TCR contact residue. Thus, in contrast with the Th1 clones that did not proliferate to A144-substituted peptide, the Th2 clones tolerated a substitution at position 144 and proliferated to A144 peptide. This alternative A144 reactive repertoire appears to have a critical role in the regulation of autoimmune response to PLP 139–151 because preimmunization with A144 to expand the L141/G142-reactive repertoire protects mice from developing EAE induced with the native PLP 139–151 peptide. These data suggest that a balance between two different T cell repertoires specific for same autoantigenic epitope can determine disease phenotype, i.e., resistance or susceptibility to an autoimmune disease.

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