Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection.
C-type lectin receptors (CLRs) are diverse, trans-membrane proteins that function as pattern recognition receptors (PRRs) which are necessary for orchestrating immune responses against pathogens. CLRs have been shown to play a major role in recognition and protection against fungal pathogens. Dectin...
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2017-01-01
|
| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC5249099?pdf=render |
| _version_ | 1819108335407857664 |
|---|---|
| author | Althea Campuzano Natalia Castro-Lopez Karen L Wozniak Chrissy M Leopold Wager Floyd L Wormley |
| author_facet | Althea Campuzano Natalia Castro-Lopez Karen L Wozniak Chrissy M Leopold Wager Floyd L Wormley |
| author_sort | Althea Campuzano |
| collection | DOAJ |
| description | C-type lectin receptors (CLRs) are diverse, trans-membrane proteins that function as pattern recognition receptors (PRRs) which are necessary for orchestrating immune responses against pathogens. CLRs have been shown to play a major role in recognition and protection against fungal pathogens. Dectin-3 (also known as MCL, Clecsf8, or Clec4d) is a myeloid cell-specific CLR that recognizes mycobacterial trehalose 6,6'-dimycolate (TDM) as well as α-mannans present in the cell wall of fungal pathogens. To date, a potential role for Dectin-3 in the mediation of protective immune responses against C. neoformans has yet to be determined. Consequently, we evaluated the impact of Dectin-3 deficiency on the development of protective immune responses against C. neoformans using an experimental murine model of pulmonary cryptococcosis. Dectin-3 deficiency did not lead to increased susceptibility of mice to experimental pulmonary C. neoformans infection. Also, no significant differences in pulmonary leukocyte recruitment and cytokine production were observed in Dectin-3 deficient mice compared to wild type infected mice. In addition, we observed no differences in uptake and anti-cryptococcal activity of Dectin-3 deficient dendritic cells and macrophages. Altogether, our studies show that Dectin-3 is dispensable for mediating protective immune responses against pulmonary C. neoformans infection. |
| first_indexed | 2024-12-22T03:08:18Z |
| format | Article |
| id | doaj.art-180d81c69f9d431ca7bacb379b35e34a |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-22T03:08:18Z |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-180d81c69f9d431ca7bacb379b35e34a2022-12-21T18:40:59ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01121e016934710.1371/journal.pone.0169347Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection.Althea CampuzanoNatalia Castro-LopezKaren L WozniakChrissy M Leopold WagerFloyd L WormleyC-type lectin receptors (CLRs) are diverse, trans-membrane proteins that function as pattern recognition receptors (PRRs) which are necessary for orchestrating immune responses against pathogens. CLRs have been shown to play a major role in recognition and protection against fungal pathogens. Dectin-3 (also known as MCL, Clecsf8, or Clec4d) is a myeloid cell-specific CLR that recognizes mycobacterial trehalose 6,6'-dimycolate (TDM) as well as α-mannans present in the cell wall of fungal pathogens. To date, a potential role for Dectin-3 in the mediation of protective immune responses against C. neoformans has yet to be determined. Consequently, we evaluated the impact of Dectin-3 deficiency on the development of protective immune responses against C. neoformans using an experimental murine model of pulmonary cryptococcosis. Dectin-3 deficiency did not lead to increased susceptibility of mice to experimental pulmonary C. neoformans infection. Also, no significant differences in pulmonary leukocyte recruitment and cytokine production were observed in Dectin-3 deficient mice compared to wild type infected mice. In addition, we observed no differences in uptake and anti-cryptococcal activity of Dectin-3 deficient dendritic cells and macrophages. Altogether, our studies show that Dectin-3 is dispensable for mediating protective immune responses against pulmonary C. neoformans infection.http://europepmc.org/articles/PMC5249099?pdf=render |
| spellingShingle | Althea Campuzano Natalia Castro-Lopez Karen L Wozniak Chrissy M Leopold Wager Floyd L Wormley Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection. PLoS ONE |
| title | Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection. |
| title_full | Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection. |
| title_fullStr | Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection. |
| title_full_unstemmed | Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection. |
| title_short | Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection. |
| title_sort | dectin 3 is not required for protection against cryptococcus neoformans infection |
| url | http://europepmc.org/articles/PMC5249099?pdf=render |
| work_keys_str_mv | AT altheacampuzano dectin3isnotrequiredforprotectionagainstcryptococcusneoformansinfection AT nataliacastrolopez dectin3isnotrequiredforprotectionagainstcryptococcusneoformansinfection AT karenlwozniak dectin3isnotrequiredforprotectionagainstcryptococcusneoformansinfection AT chrissymleopoldwager dectin3isnotrequiredforprotectionagainstcryptococcusneoformansinfection AT floydlwormley dectin3isnotrequiredforprotectionagainstcryptococcusneoformansinfection |