Francys Avendaño-Rangel
Research Subjects
Research Interests
Francys Avendaño-Rangel has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Camila Indiani de Oliveira
Instituto Gonçalo Muniz, FIOCRUZ, Salvador, BA, Brazil; Instituto Nacional de Ciência e Tecnologia em Doenças Tropicais (INCT-DT), Salvador, Bahia, Brazil
1 shared publication - Gabriela Agra-Duarte
Instituto Gonçalo Moniz, FIOCRUZ, Salvador 40296-710, BA, Brazil
1 shared publication - Hira L. Nakhasi
Division of Emerging and Transfusion Transmitted Diseases, CBER, FDA, Silver Spring, MD, USA
1 shared publication - Larissa O. da Silva
Instituto Gonçalo Moniz, FIOCRUZ, Salvador 40296-710, BA, Brazil
1 shared publication - Leslye T. Avila
Instituto Gonçalo Moniz, FIOCRUZ, Salvador 40296-710, BA, Brazil
1 shared publication - Pedro B. Borba
Instituto Gonçalo Moniz, FIOCRUZ, Salvador 40296-710, BA, Brazil
1 shared publication
Latest Publications
- Open Access
Immunization with centrin-Deficient Leishmania braziliensis Does Not Protect against Homologous Challenge
Immunization with various Leishmania species lacking centrin induces robust immunity against a homologous and heterologous virulent challenge, making centrin mutants a putative candidate for a leishmaniasis vaccine. Centrin is a calcium-binding cytoskeletal protein involved in centrosome duplication in higher eukaryotes and Leishmania spp. lacking centrin are unable to replicate in vivo and are non-pathogenic. We developed a centrin-deficient Leishmania braziliensis (LbCen−/−) cell line and confirmed its impaired survival following phagocytosis by macrophages. Upon experimental inoculation into BALB/c mice, LbCen−/− failed to induce lesions and parasites were rapidly eliminated. The immune response following inoculation with LbCen−/− was characterized by a mixed IFN-γ, IL-4, and IL-10 response and did not confer protection against L. braziliensis infection, distinct from L. major, L. donovani, and L mexicana centrin-deficient mutants. A prime-boost strategy also did not lead to a protective immune response against homologous challenge. On the contrary, immunization with centrin-deficient L. donovani (LdonCen−/−) cross-protected against L. braziliensis challenge, illustrating the ability of LdonCen−/− to induce the Th1-dominant protective immunity needed for leishmaniasis control. In conclusion, while centrin deficiency in L. braziliensis causes attenuation of virulence, and disrupts the ability to cause disease, it fails to stimulate a protective immune response.
Open AccessImmunization with centrin-Deficient Leishmania braziliensis Does Not Protect against Homologous Challenge
Immunization with various Leishmania species lacking centrin induces robust immunity against a homologous and heterologous virulent challenge, making centrin mutants a putative candidate for a leishmaniasis vaccine. Centrin is a calcium-binding cytoskeletal protein involved in centrosome duplication in higher eukaryotes and Leishmania spp. lacking centrin are unable to replicate in vivo and are non-pathogenic. We developed a centrin-deficient Leishmania braziliensis (LbCen−/−) cell line and confirmed its impaired survival following phagocytosis by macrophages. Upon experimental inoculation into BALB/c mice, LbCen−/− failed to induce lesions and parasites were rapidly eliminated. The immune response following inoculation with LbCen−/− was characterized by a mixed IFN-γ, IL-4, and IL-10 response and did not confer protection against L. braziliensis infection, distinct from L. major, L. donovani, and L mexicana centrin-deficient mutants. A prime-boost strategy also did not lead to a protective immune response against homologous challenge. On the contrary, immunization with centrin-deficient L. donovani (LdonCen−/−) cross-protected against L. braziliensis challenge, illustrating the ability of LdonCen−/− to induce the Th1-dominant protective immunity needed for leishmaniasis control. In conclusion, while centrin deficiency in L. braziliensis causes attenuation of virulence, and disrupts the ability to cause disease, it fails to stimulate a protective immune response.