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Dive into the research topics where Marta Rodriguez-Garcia is active.

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Featured researches published by Marta Rodriguez-Garcia.


American Journal of Reproductive Immunology | 2010

Peripheral Blood Cytokine Profiling During Pregnancy and Post-partum Periods

Thomas Kraus; Rhoda S. Sperling; Stephanie M. Engel; Yungtai Lo; Lisa Kellerman; Tricia Singh; Martine Loubeau; Yongchao Ge; Jose Luis Garrido; Marta Rodriguez-Garcia; Thomas M. Moran

Citation Kraus TA, Sperling RS, Engel SM, Lo Y, Kellerman L, Singh T, Loubeau M, Ge Y, Garrido JL, Rodríguez‐García M, Moran TM. Peripheral blood cytokine profiling during pregnancy and post‐partum periods. Am J Reprod Immunol 2010; 64: 411–426


PLOS ONE | 2010

Increased α-defensins 1-3 production by dendritic cells in HIV-infected individuals is associated with slower disease progression.

Marta Rodriguez-Garcia; Núria Climent; Harold Oliva; Víctor Casanova; Rafael Franco; Agathe León; José M. Gatell; Felipe García; Teresa Gallart

Background Defensins are natural endogenous antimicrobial peptides with potent anti-HIV activity and immuno-modulatory effects. We recently demonstrated that immature dendritic cells (DC) produce α-defensins1-3 and that α-defensins1-3 modulate DC generation and maturation. Since DC-HIV interaction plays a critical role during the first steps of HIV infection, we investigated the possible impact of α-defensins1-3 production by DC on disease progression. Methodology/Principal Findings Monocyte-derived DC (MDDC) were analyzed comparatively in healthy controls (HC) and HIV-infected patients, including untreated “elite” and “viremic” controllers, untreated viremic non-controllers and antiretroviral-treated patients. We found that production of α-defensins1-3 was significantly increased in MDDC from HIV-infected patients versus HC, and this increase was mainly due to that observed in controllers, while in non-controllers the increase was not statistically significant (controllers vs. HC, p<0.005; controllers vs. non-controllers p<0.05). Secreted α-defensins1-3 by immature MDDC positively correlated with CD4 T cell counts in controllers, but not in non-controllers. Moreover, independently of their clinical classification, HIV-infected patients with higher α-defensins1-3 secretion by immature MDDC showed slower disease progression, measured as no decrease in the number of CD4+ T-cells below 350 cell/mm3, lower increase of plasma viral load and no initiation of treatment over time. Plasma alpha-defensins1-3 levels lacked any relationship with immunologic and virologic parameters. Conclusions/Significance High production of α-defensins1-3 by immature DCs appears as a host protective factor against progression of HIV-1infection, suggesting potential diagnostic, therapeutic and preventive implications. This protective effect may arise from the activity of α-defensins1-3 to damage the virions prior and/or after their internalization by immature DC, and hence favoring a more efficient viral processing and presentation to HIV-specific CD4+ T cells, without or with a minor rate of transmission of infectious HIV-1 virions.


Mucosal Immunology | 2014

Phenotype and susceptibility to HIV infection of CD4+ Th17 cells in the human female reproductive tract.

Marta Rodriguez-Garcia; Fiona D. Barr; Sarah G. Crist; John V. Fahey; Charles R. Wira

Prevention of sexual acquisition of HIV in women requires a substantial increase in our knowledge about HIV-target cell availability and regulation in the female reproductive tract (FRT). In this study, we analyzed the phenotype and susceptibility to HIV infection of CD4+ T cell in the endometrium (EM), endocervix (END), and ectocervix (ECT) of the FRT. We found that T helper type 17 (Th17) cells represent a major subset in FRT tissues analyzed and that Th17 cells were the main CD4+ T-cell population expressing C-C motif chemokine receptor 5 (CCR5) and CD90. In premenopausal women, CD4+ T cells and Th17 cells, in particular, were significantly lower in EM relative to END and ECT. Th17 cells were elevated in EM from postmenopausal women relative to premenopausal tissues but not changed in END and ECT. Susceptibility of CD4+ T cells to HIV infection measured as intracellular p24 was lowest in the EM and highest in the ECT. Additionally, we found that Th17 cells co-expressing CCR5 and CD90 were the most susceptible to HIV infection. Our results provide valuable information for designing preventive strategies directed at targeting highly susceptible target cells in the FRT.


PLOS ONE | 2013

Estradiol Reduces Susceptibility of CD4 + T Cells and Macrophages to HIV-Infection

Marta Rodriguez-Garcia; Nabanita Biswas; Mickey V. Patel; Fiona D. Barr; Sarah G. Crist; Christina Ochsenbauer; John V. Fahey; Charles R. Wira

The magnitude of the HIV epidemic in women requires urgent efforts to find effective preventive methods. Even though sex hormones have been described to influence HIV infection in epidemiological studies and regulate different immune responses that may affect HIV infection, the direct role that female sex hormones play in altering the susceptibility of target cells to HIV-infection is largely unknown. Here we evaluated the direct effect of 17-β-estradiol (E2) and ethinyl estradiol (EE) in HIV-infection of CD4+ T-cells and macrophages. Purified CD4+ T-cells and monocyte-derived macrophages were generated in vitro from peripheral blood and infected with R5 and X4 viruses. Treatment of CD4+ T-cells and macrophages with E2 prior to viral challenge reduced their susceptibility to HIV infection in a dose-dependent manner. Addition of E2 2 h after viral challenge however did not result in reduced infection. In contrast, EE reduced infection in macrophages to a lesser extent than E2 and had no effect on CD4+ T-cell infection. Reduction of HIV-infection induced by E2 in CD4+ T-cells was not due to CCR5 down-regulation, but was an entry-mediated mechanism since infection with VSV-G pseudotyped HIV was not modified by E2. In macrophages, despite the lack of an effect of E2 on CCR5 expression, E2–treatment reduced viral entry 2 h after challenge and increased MIP-1β secretion. These results demonstrate the direct effect of E2 on susceptibility of HIV-target cells to infection and indicate that inhibition of target cell infection involves cell-entry related mechanisms.


American Journal of Reproductive Immunology | 2014

Regulation of Mucosal Immunity in the Female Reproductive Tract: The Role of Sex Hormones in Immune Protection Against Sexually Transmitted Pathogens

Charles R. Wira; John V. Fahey; Marta Rodriguez-Garcia; Zheng Shen; Mickey V. Patel

The immune system in the female reproductive tract (FRT) does not mount an attack against human immunodeficiency virus (HIV) or other sexually transmitted infections (STI) with a single endogenously produced microbicide or with a single arm of the immune system. Instead, the body deploys dozens of innate antimicrobials to the secretions of the FRT. Working together, these antimicrobials along with mucosal antibodies attack viral, bacterial, and fungal targets. Within the FRT, the unique challenges of protection against sexually transmitted pathogens coupled with the need to sustain the development of an allogeneic fetus, has evolved in such a way that sex hormones precisely regulate immune function to accomplish both tasks. The studies presented in this review demonstrate that estradiol (E2) and progesterone secreted during the menstrual cycle act both directly and indirectly on epithelial cells, fibroblasts and immune cells in the reproductive tract to modify immune function in a way that is unique to specific sites throughout the FRT. As presented in this review, studies from our laboratory and others demonstrate that the innate and adaptive immune systems are under hormonal control, that protection varies with the stage of the menstrual cycle and as such, is dampened during the secretory stage of the cycle to optimize conditions for fertilization and pregnancy. In doing so, a window of STI vulnerability is created during which potential pathogens including HIV enter the reproductive tract to infect host targets.


Mucosal Immunology (Fourth Edition) | 2015

Endocrine Regulation of the Mucosal Immune System in the Female Reproductive Tract

Charles R. Wira; Marta Rodriguez-Garcia; Mickey V. Patel; Nabanita Biswas; John V. Fahey

Abstract Ovarian sex hormones have a critical role in regulating all aspects of the mucosal immune system of the human and animal female reproductive tract. Consisting of the innate and adaptive immune systems, the upper (fallopian tubes, uterus, and endocervix) and lower (ectocervix and vagina) systems are precisely regulated by estradiol (E 2 ) and progesterone (P 4 ) to optimize conditions for successful pregnancy and protection against sexually transmitted diseases. This review aims to examine the effects of E 2 and P 4 on innate, humoral, and cellular immunity in the reproductive tracts of human and rodent, pointing out unique similarities and differences that exist in terms of immune cell distribution and function, chemokine, cytokine and antimicrobial secretion, immunoglobulin production and transport, and antigen presentation. The studies presented indicate that endocrine control of immune system in the upper and lower reproductive tract is separate and distinct and that immune function at each site must be analyzed in the context of the unique contributions that each makes to procreation and to maternal and fetal protection against potential pathogens.


Arthritis & Rheumatism | 2008

The rheumatoid arthritis–associated allele HLA–DR10 (DRB1*1001) shares part of its repertoire with HLA–DR1 (DRB1*0101) and HLA–DR4 (DRB*0401)

Iñaki Alvarez; Javier Collado; Xavier Daura; Núria Colomé; Marta Rodriguez-Garcia; Teresa Gallart; Francesc Canals; Dolores Jaraquemada

OBJECTIVE To identify the peptide anchor motif for the rheumatoid arthritis (RA)-related HLA allele, DR10, and find shared natural ligands or sequence similarities with the other disease-associated alleles, DR1 and DR4. METHODS The HLA-DR10-associated peptides were purified, and a proportion of these natural ligands were de novo sequenced by mass spectrometry. Based on crystallographic structures, the complexes formed by peptide influenza virus hemagglutinin HA306-318 with DR1, DR4, and DR10 were modeled, and binding scores were obtained. RESULTS A total of 238 peptides were sequenced, and the anchor motif of the HLA-DR10 peptide repertoire was defined. A large proportion of the DR10-associated peptides had the structural features to bind DR1 and DR4 but were theoretical nonbinders to the negatively associated alleles DR15 and DR7. Among the sequenced ligands, 10 had been reported as ligands to other RA-associated alleles. Modeling data showed that peptide HA306-318 can bind DR1, DR4, and DR10 with similar affinities. CONCLUSION The data show the presence of common peptides in the repertoires of RA-associated HLA alleles. The combination of the shared epitope present in DR1, DR4, and DR10 together with common putative arthritogenic peptide(s) could influence disease onset or outcome.


American Journal of Reproductive Immunology | 2013

Immunobiology of Genital Tract Trauma: Endocrine Regulation of HIV Acquisition in Women Following Sexual Assault or Genital Tract Mutilation

Mimi Ghosh; Marta Rodriguez-Garcia; Charles R. Wira

Studies on HIV acquisition and transmission in women exposed to sexual trauma throughout their life cycle are lacking, but some findings suggest that rates of HIV acquisition through coercive sex are significantly higher than that seen in consensual sex. Sexual trauma can also occur as a result of female genital mutilation, which makes sex extremely painful and can cause increased abrasions, lacerations, and inflammation, which enhances the risk of HIV acquisition. This review presents an overview of the immune system in the human female reproductive tract (FRT) from adolescence, through puberty to pregnancy and menopause. What is clear is that the foundation of information on immune protection in the FRT throughout the life cycle of women is extremely limited and at some stages such as adolescence and menopause are grossly lacking. Against this backdrop, forced or coercive sexual intercourse as well as genital mutilation further complicates our understanding of the biological risk factors that can result in transmission of HIV and other sexually transmitted infections.


PLOS ONE | 2014

Sex Hormones Regulate Tenofovir-Diphosphate in Female Reproductive Tract Cells in Culture

Zheng Shen; John V. Fahey; Jack E. Bodwell; Marta Rodriguez-Garcia; Angela D. M. Kashuba; Charles R. Wira

The conflicting results of recent pre-exposure prophylaxis (PrEP) trials utilizing tenofovir (TFV) to prevent HIV infection in women led us to evaluate the accumulation of intracellular TFV-diphosphate (TFV-DP) in cells from the female reproductive tract (FRT) and whether sex hormones influence the presence of TFV-DP in these cells. Following incubation with TFV, isolated epithelial cells, fibroblasts, CD4+ T cells and CD14+ cells from the FRT as well as blood CD4+ T cells and monocyte-derived macrophages convert TFV to TFV-DP. Unexpectedly, we found that TFV-DP concentrations (fmol/million cells) vary significantly with the cell type analyzed and the site within the FRT. Epithelial cells had 5-fold higher TFV-DP concentrations than fibroblasts; endometrial epithelial cells had higher TFV-DP concentrations than cells from the ectocervix. Epithelial cells had 125-fold higher TFV-DP concentrations than FRT CD4+ T cells, which were comparable to that measured in peripheral blood CD4+ T cells. These findings suggest the existence of a TFV-DP gradient in the FRT where epithelial cells > fibroblasts > CD4+ T cells and macrophages. In other studies, estradiol increased TFV-DP concentrations in endometrial and endocervical/ectocervical epithelial cells, but had no effect on fibroblasts or CD4+ T cells from FRT tissues. In contrast, progesterone alone and in combination with estradiol decreased TFV-DP concentrations in FRT CD4+ T cells. Our results suggest that epithelial cells and fibroblasts are a repository of TFV-DP that is under hormonal control. These cells might act either as a sink to decrease TFV availability to CD4+ T cells and macrophages in the FRT, or upon conversion of TFV-DP to TFV increase TFV availability to HIV-target cells. In summary, these results indicate that intracellular TFV-DP varies with cell type and location in the FRT and demonstrate that estradiol and/or progesterone regulate the intracellular concentrations of TFV-DP in FRT epithelial cells and CD4+ T cells.


Reproductive Biology and Endocrinology | 2011

Alpha-defensins 1-3 release by dendritic cells is reduced by estrogen

Maria M. Escribese; Marta Rodriguez-Garcia; Rhoda S. Sperling; Stephanie M. Engel; Teresa Gallart; Thomas M. Moran

BackgroundDuring pregnancy the immune system of the mother must protect any activation that may negatively affect the fetus. Changes in susceptibility to infection as well as resolution of some autoimmune disorders represent empirical evidence for pregnancy related alterations in immunity. Sex hormones reach extremely high levels during pregnancy and have been shown to have direct effects on many immune functions including the antiviral response of dendritic cells. Among the immunologically active proteins secreted by monocyte derived DCs (MDDC) are the alpha-defensins 1-3. This family of cationic antimicrobial peptides has a broad spectrum of microbicidal activity and has also been shown to link innate to adaptive immunity by attracting T cells and immature DCs, which are essential for initiating and polarizing the immune response.MethodsWe compare culture-generated monocyte derived DCs (MDDCs) with directly isolated myeloid dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs) and measure their alpha-defensins 1-3 secretion by ELISA both, in basal situations and after hormone (E2 or PG) treatments. Moreover, using a cohort of pregnant women we isolated mDCs from blood and also measure the levels of these anti-microbial peptides along pregnancy.ResultsWe show that mDCs and pDCs constitutively produce alpha-defensins 1-3 and at much higher levels than MDDCs. Alpha-defensins 1-3 production from mDCs and MDDCs but not pDCs is inhibited by E2. PG does not affect alpha-defensins 1-3 in any of the populations. Moreover, alpha-defensins 1-3 production by mDCs was reduced in the later stages of pregnancy in 40% of the patients.ConclusionsHere, we demonstrate that mDCs and pDCs secrete alpha-defensins 1-3 and present a novel effect of E2 on the secretion of alpha-defensins 1-3 by dendritic cells.

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Christina Ochsenbauer

University of Alabama at Birmingham

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