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Cat. No.: HY-P5462

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PLP (180-199)

PLP (180-199) is a myelin proteolipid protein-derived peptide corresponding to amino acids 180-199 of PLP. PLP (180-199) acts as an encephalitogenic peptide and induces experimental autoimmune encephalomyelitis (EAE) in susceptible BALB/c mice. PLP (180-199) can stimulate antigen-specific T-cell responses, promote inflammatory cytokine production including IFN-γ and TNF-α, and is used for the study of autoimmune encephalomyelitis and multiple sclerosis-related immune responses.

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CAS No.: 165549-58-6
Formule: C₉₂H₁₄₅N₂₃O₃₀S
Masse moléculaire:2085.34

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Please store the product under the recommended conditions in the Certificate of Analysis.

PLP (180-199) Chemical Structure

CAS No.: 165549-58-6

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Activité biologique
- Description
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
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Classifications
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Activité biologique

Description

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In Vitro

PLP (180-199) stimulates antigen-specific lymphocyte proliferation in spleen and lymph node cells isolated from PLP180-199-immunized BALB/c mice after peptide restimulation^[1].
PLP (180-199) (10 μg/mL) induces IFN-γ and TNF-α production in lymphoid cells isolated from PLP180-199-immunized BALB/c mice after peptide stimulation^[2].
PLP (180-199) (10-14 days after immunization) stimulates proliferation and IFN-γ production of spleen and lymph node cells from wild-type and B cell-deficient BALB/c mice after PLP180-199 immunization^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

PLP (180-199) (200 μg/mouse; s.c.; emulsified with IFA containing 0.5 mg/mouse Mycobacterium tuberculosis H37RA; pertussis toxin 300 ng i.v. at immunization and 72 h later) induces experimental autoimmune encephalomyelitis (EAE) in female BALB/c mice after subcutaneous immunization with peptide emulsified in adjuvant, resulting in clinical paralysis and CNS inflammatory pathology^[1].
PLP (180-199) (200 μg/mouse; s.c. immunization) induces EAE in BALB/c mice with increased clinical disease scores and characteristic ascending paralysis^[2].
PLP (180-199) (200 μg/mouse; s.c. immunization) induces EAE in wild-type and B cell-deficient BALB/c mice and regulates disease severity through antigen-specific immune responses^[3].

Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

1. Experimental Autoimmune Encephalomyelitis (EAE) Model^[1]^[2]^[3]

Background

PLP (180-199) peptide induces autoimmune responses against myelin proteins, activating autoreactive T cells and causing inflammatory demyelinating lesions in the central nervous system, thereby inducing EAE^[1]^[2]^[3].

Specific Modeling Methods

Mice: Female•BALB/c mice•(6-8 weeks old)
Administration: PLP (180-199) peptide (200 μg/mouse) emulsified 1:1 in incomplete Freund’s adjuvant (IFA) containing Mycobacterium tuberculosis H37Ra (0.5 mg/mouse; 0.1 mL emulsion/mouse)•administered subcutaneously (s.c.) at immunization sites. Pertussis toxin (300 ng/mouse) was injected intravenously (i.v.) at the time of immunization and 72 h later to induce EAE

Note

(1) PLP (180-199) peptide should be emulsified with incomplete Freund’s adjuvant containing Mycobacterium tuberculosis H37RA before subcutaneous immunization.
(2) Pertussis toxin administration is required for EAE induction and was given intravenously at immunization and 72 h later.
(3) Clinical EAE severity was evaluated using a clinical scoring system based on paralysis progression.

Modeling Indicators

Clinical assessment: Clinical EAE score, including ascending paralysis symptoms such as limp tail, hind limb weakness/paralysis and forelimb involvement.
Histology analysis: Inflammatory cell infiltration, demyelination, and axonal loss in the central nervous system.
Immune response analysis:Increased PLP-specific T cell responses and altered cytokine production, including IFN-γ and IL-10 changes.

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Chemical Information

CAS No. 165549-58-6
Masse moléculaire 2085.34
Formule C₉₂H₁₄₅N₂₃O₃₀S
Sequence

Trp-Thr-Thr-Cys-Gln-Ser-Ile-Ala-Phe-Pro-Ser-Lys-Thr-Ser-Ala-Ser-Ile-Gly-Ser-Leu
Sequence Shortening

WTTCQSIAFPSKTSASIGSL
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

Fiche technique (285 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Instruction de manipulation (2659 KB)

Références

[1]. Lyons JA, et al., B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice. J Autoimmun. 2008 Sep;31(2):149-55. [Content Brief]

[2]. Lyons JA, et al. Identification of the Encephalitogenic Epitopes of CNS Proteolipid Protein in BALB/c Mice. Journal of Autoimmunity. 2002;19:195–201.

[3]. Nath N, et al. T-bet is essential for the progression of experimental autoimmune encephalomyelitis. Immunology. 2006;118:384–391.

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Activité biologique
- Description
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références

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PLP (180-199)

Voir tous les produits spécifiques à Isoform TNF Receptor