Laura Contreras-Ruiz
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Laura Contreras-Ruiz has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Alyssa Rocha
Department of Experimental Medicine, Dana-Farber Cancer Institute, Boston, Massachusetts, USA
1 shared publication - Arpita Ghosh Mitra
Rajiv Gandhi Cancer Institute and research Centre, New Delhi 110085, India
1 shared publication D. A. Dartt
Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear, Boston, MA 02114, USA
1 shared publication- Eva Guinan
DF/CH Hematopoietic Stem Cell Transplant Program, Dana-Farber Cancer Institute, USA
1 shared publication M. A. Shatos
Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear, Boston, MA 02114, USA
1 shared publication- Rakesh Rudraboina
Department of Experimental Medicine, Dana-Farber Cancer Institute, Boston, Massachusetts, USA
1 shared publication
Latest Publications
- Open Access
- 9 July 2024
- Published by Elsevier in American Journal of Transplantation
- Vol. 24 (11) , 1968-1978
Allostimulation leads to emergence of a human B cell population with increased expression of HLA class I antigen presentation–associated molecules and the immunoglobulin receptor FcRL5
- 9 July 2024
- Published by Elsevier in American Journal of Transplantation
- Vol. 24 (11) , 1968-1978
Open AccessAllostimulation leads to emergence of a human B cell population with increased expression of HLA class I antigen presentation–associated molecules and the immunoglobulin receptor FcRL5
- Open Access
- 17 December 2013
- Published by Wiley in Mediators of Inflammation
- Vol. 2013, 1-11
Modulation of Conjunctival Goblet Cell Function by Inflammatory Cytokines
Ocular surface inflammation associated with Sjögren’s syndrome is characterized by a loss of secretory function and alteration in numbers of mucin secreting goblet cells. Such changes are a prominent feature of ocular surface inflammatory diseases and are attributed to inflammation; however, the exact effect of the inflammatory cytokines on conjunctival goblet cell function remains largely unknown. In this study, we developed a primary culture of mouse goblet cells from conjunctival tissue and evaluated the effects on their function by inflammatory cytokines detected in the conjunctiva of mouse model of Sjögren’s syndrome (Thrombospondin-1 deficient mice). We found that apoptosis of goblet cells was primarily induced by TNF-αand IFN-γ. These two cytokines also inhibited mucin secretion by goblet cells in response to cholinergic stimulation, whereas IL-6 enhanced such secretion. No changes in secretory response were detected in the presence of IL-13 or IL-17. Goblet cells proliferated to varying degrees in response to all the tested cytokines with the greatest response to IL-13 followed by IL-6. Our results therefore reveal that inflammatory cytokines expressed in the conjunctiva during an ocular surface disease directly disrupt conjunctival goblet cell functions, compromising the protective function of tears, thereby contributing to ocular surface damage.
- 17 December 2013
- Published by Wiley in Mediators of Inflammation
- Vol. 2013, 1-11
Open AccessModulation of Conjunctival Goblet Cell Function by Inflammatory Cytokines
Ocular surface inflammation associated with Sjögren’s syndrome is characterized by a loss of secretory function and alteration in numbers of mucin secreting goblet cells. Such changes are a prominent feature of ocular surface inflammatory diseases and are attributed to inflammation; however, the exact effect of the inflammatory cytokines on conjunctival goblet cell function remains largely unknown. In this study, we developed a primary culture of mouse goblet cells from conjunctival tissue and evaluated the effects on their function by inflammatory cytokines detected in the conjunctiva of mouse model of Sjögren’s syndrome (Thrombospondin-1 deficient mice). We found that apoptosis of goblet cells was primarily induced by TNF-αand IFN-γ. These two cytokines also inhibited mucin secretion by goblet cells in response to cholinergic stimulation, whereas IL-6 enhanced such secretion. No changes in secretory response were detected in the presence of IL-13 or IL-17. Goblet cells proliferated to varying degrees in response to all the tested cytokines with the greatest response to IL-13 followed by IL-6. Our results therefore reveal that inflammatory cytokines expressed in the conjunctiva during an ocular surface disease directly disrupt conjunctival goblet cell functions, compromising the protective function of tears, thereby contributing to ocular surface damage.