plp (139 151)

PLP (139-151), an amino acid residue from positions 139 to 151 of myelin proteolipid protein (PLP), is utilized to induce the relapsing-remitting (RR)-EAE model.

[Leu144,Arg147]-PLP (139-151) is a mutated fragment of the myelin proteolipid protein (PLP), featuring substitutions of tryptophan to leucine and histidine to arginine at positions 144 and 147, respectively. Immunizing mice with this peptide (50 µg) mixed in complete Freund's adjuvant (CFA) elevates IL-4 levels in the spleen. While it suppresses Th1 cell activation in vitro, it does not do so in vivo; instead, it promotes the development of regulatory T cells. Preimmunization with [Leu144, Arg147]-PLP (139-151) postpones the onset of experimental autoimmune encephalomyelitis (EAE) triggered by encephalitogenic peptides from PLP (178-191), myelin oligodendrocyte glycoprotein (MOG) (92-106), or myelin basic protein (MBP) in mice.

[SER140]-PLP(139-151) is a polypeptide fragment derived from the myelin-associated lipid protein.

[SER140]-PLP(139-151) acetate is a peptide fragment from myelin proteolipid protein (PLP).

[SER140]-PLP(139-151) (TFA) is a polypeptide fragment of the myelin lipid protein.

PLP (178-191), an immunodominant encephalitogenic epitope from the proteolipid protein (PLP) fragment spanning amino acids 178 to 191, plays a pivotal role in SJL mice. It initiates disease onset earlier compared to the other major encephalitogenic epitope, PLP (139-151), though both epitopes result in similar incidence, severity, and histologic characteristics.

J5 peptide, an MBP inhibitor, competitively inhibits the binding of MBP 85-99 to HLA-DR2, and mitigates PLP 139-151 MBP 85-99-induced experimental autoimmune encephalomyelitis (EAE) in mice. It is utilized in research pertaining to inflammatory and immune diseases [1].