H-His-Cys-Leu-Gly-Lys-Trp-Leu-Gly-His-Pro-Asp-Lys-Phe-OH

Product NameH-His-Cys-Leu-Gly-Lys-Trp-Leu-Gly-His-Pro-Asp-Lys-Phe-OH
CAS131334-43-5
MFC72H104N20O16S
MW1537.79
EINECS
MOL File131334-43-5.mol

Chemical Properties

Boiling point	1897.4±65.0 °C(Predicted)
Density	1.332±0.06 g/cm3(Predicted)
pka	3.49±0.10(Predicted)
form	White to off-white powder.
color	White to off-white
Sequence	H-His-Cys-Leu-Gly-Lys-Trp-Leu-Gly-His-Pro-Asp-Lys-Phe-OH

Usage And Synthesis

Uses

PLP (139-151) is amino acid residue 139 to 151 of myelin proteolipid protein (PLP) used to induce experimental autoimmune encephalomyelitis (EAE).

in vivo

PLP (139-151) can be used in animal modeling to create relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) models. The pro-inflammatory cytokine IL-17 plays a crucial role in the PLP (139-151)-induced encephalomyelitis process. After subcutaneous injection of PLP (139-151) into mice, CD4 cells that specifically respond to PLP (139-151) and release pro-inflammatory cytokines migrate to and accumulate in the damaged central nervous system (CNS) regions^[4]^[5].

Induction of Relapsing-Remitting Experimental Autoimmune Encephalomyelitis (RR-EAE)

Background

Proinflammatory cytokines produced by neuroantigen-specific T cells are considered key factors in the initiation and maintenance of autoimmune encephalomyelitis. PLP (139-151) induces autoimmune encephalomyelitis by activating immune responses mediated by specific CD4 cells, which release proinflammatory cytokines such as IL-17 and IFN-γ. This leads to local inflammation and disruption of neural function, thereby inducing autoimmune encephalomyelitis^[5]^[6].

Specific Modeling Methods

Mice: SJL/J female 6-week-old
Administration: 100 μg sc single dose

Note

1. Subcutaneously inject 100 μg of PLP (139-151) (100 μl, 1 μg/μl) along with 100 μl of complete Freund's adjuvant (HY-153808) to enhance the mouse's immune response to PLP (139-151).
2. One day after the subcutaneous injection of PLP (139-151), perform an intraperitoneal injection of 100 μl (2 ng/μl, dissolved in phosphate-buffered saline (PBS)) of Bordetella pertussis toxin (BPX) to further enhance the mouse's immune response to PLP (139-151).
3. Monitor the mice daily for changes in body weight and clinical status. Perform neurological evaluations using a clinical score (CS) system with the following scale: 0 for no abnormalities; 0.5 for a drooping tail tip; 1 for a limp tail; 1.5 for hind limb dysfunction; 2 for hind limb weakness; 2.5 for dragging hind limbs; 3 for hind limb paralysis; 3.5 for complete hind limb paralysis with the mouse unable to right itself when placed on its side; and 4 for complete hind limb paralysis and partial front limb paralysis.
4. Isolate mice with early clinical symptoms of encephalomyelitis in separate cages with easier access to food and water. Dehydrated mice should receive an intraperitoneal injection of saline solution at least once a day.

Modeling Indicators

Phenotypic Observations: Resulted mouse weight loss and a significant increase in clinical scores.
Histological Changes: Resulted iron deposits in the cerebellum, medulla, and spinal cord of the mice.
Molecular Changes: Enhanced the immune signals of TSPO and Iba1 (markers of microglia and macrophage activation) in immunohistochemical results, indicating that microglia and macrophages were activated.

Correlated Product(s): Complete Freund's adjuvant (CFA) (HY-153808); Bordetella pertussis toxin

Opposite Product(s): /

References

[1] Kuchroo VK, et al. Induction of experimental allergic encephalomyelitis by myelin proteolipid-protein-specific T cell clones and synthetic peptides. Pathobiology. 1991;59(5):305-12. DOI:10.1159/000163668
[2] Sobel RA, et al. Acute experimental allergic encephalomyelitis in SJL/J mice induced by a synthetic peptide ofmyelin proteolipid protein. J Neuropathol Exp Neurol. 1990 Sep;49(5):468-79. DOI:10.1097/00005072-199009000-00002
[3] Bebo BF Jr, et al. Male SJL mice do not relapse after induction of EAE with PLP 139-151. J Neurosci Res. 1996 Sep 15;45(6):680-9. DOI:10.1002/(SICI)1097-4547(19960915)45:63.0.CO;2-4
[4] Coda AR, et al. In vivo imaging of CNS microglial activation/macrophage infiltration with combined [18F]DPA-714-PET and SPIO-MRI in a mouse model of relapsing remitting experimental autoimmune encephalomyelitis. Eur J Nucl Med Mol Imaging. 2021 Jan;48(1):40-52. DOI:10.1007/s00259-020-04842-7
[5] Turvey ME, et al. Quantitative proteome profiling of CNS-infiltrating autoreactive CD4+ cells reveals selective changes during experimental autoimmune encephalomyelitis. J Proteome Res. 2014 Aug 1;13(8):3655-70. DOI:10.1021/pr500158r
[6] Zhang H, et al. Intrinsic and induced regulation of the age-associated onset of spontaneous experimental autoimmune encephalomyelitis. J Immunol. 2008 Oct 1;181(7):4638-47. DOI:10.4049/jimmunol.181.7.4638

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