Pretreatment of leishmania homologue of receptors for activated C kinase (LACK) promotes disease progression caused by Leishmania amazonensis.

Abstract

A cDNA coding Leishmania homologue of receptors for activated C kinase (LACK), which was known to play an important role in the early phase of Leishmania infection, was molecularly cloned from Leishmania amazonensis promastigote by using reverse transcription and nested polymerase chain reaction, and was sequenced. The L. amazonenis LACK cDNA showed 97.3 to 99.3% homology and its deduced amino acid sequence showed 98.7 to 99.7% identity in comparison with LACK sequences from five other species. The amino acid sequences in the immunodominant peptide region were completely conserved among Leishmania spp. tested. Intravenous pretreatment of the recombinant L. amazonensis LACK into BALB/c mice showed progressive lesion development compared to PBS (-) injected control mice, suggesting the important role of LACK in the early phase of L. amazonensis infection.

• Authors: Takahiro Okuno, Makoto Takeuchi, Yoshitsugu Matsumoto, Haruki Otsuka, Yasunobu Matsumoto
• Journal: Experimental animals (Exp Anim) Vol. 51 Issue 4 Pg. 335-41 (Jul 2002) ISSN: 1341-1357 [Print] Japan
• PMID: 12221926 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antigens, Protozoan
• DNA, Complementary
• Protozoan Proteins
• LACK antigen, Leishmania

Topics

• Amino Acid Sequence
• Animals
• Antigens, Protozoan
• Cloning, Molecular
• DNA, Complementary (analysis)
• Disease Progression
• Leishmania
• Leishmaniasis, Cutaneous (immunology, pathology)
• Male
• Mice
• Mice, Inbred BALB C
• Polymerase Chain Reaction
• Protozoan Proteins (genetics, physiology)