Dr. Antonio Condino-Neto

@article{pmid37047078b,

title = {Photobiomodulation Reduces the Cytokine Storm Syndrome Associated with COVID-19 in the Zebrafish Model},

author = {Ivana F Rosa and Ana P B Peçanha and Tábata R B Carvalho and Leonardo S Alexandre and Vinícius G Ferreira and Lucas B Doretto and Beatriz M Souza and Rafael T Nakajima and Patrick da Silva and Ana P Barbosa and Leticia Gomes-de-Pontes and Camila G Bomfim and Glaucia M Machado-Santelli and Antonio Condino-Neto and Cristiane R Guzzo and Jean P S Peron and Magaiver Andrade-Silva and Niels O S Câmara and Anali M B Garnique and Renata J Medeiros and Fausto K Ferraris and Leonardo J G Barcellos and Jose D Correia-Junior and Jorge Galindo-Villegas and Mônica F R Machado and Angela Castoldi and Susana L Oliveira and Camila C Costa and Marco A A Belo and Giovane Galdino and Germán G Sgro and Natalia F Bueno and Silas F Eto and Flávio P Veras and Bianca H V Fernandes and Paulo R S Sanches and Eduardo M Cilli and Guilherme Malafaia and Rafael H Nóbrega and Aguinaldo S Garcez and Emanuel Carrilho and Ives Charlie-Silva},

doi = {10.3390/ijms24076104},

issn = {1422-0067},

year  = {2023},

date = {2023-03-01},

journal = {Int J Mol Sci},

volume = {24},

number = {7},

abstract = {Although the exact mechanism of the pathogenesis of coronavirus SARS-CoV-2 (COVID-19) is not fully understood, oxidative stress and the release of pro-inflammatory cytokines have been highlighted as playing a vital role in the pathogenesis of the disease. In this sense, alternative treatments are needed to reduce the level of inflammation caused by COVID-19. Therefore, this study aimed to investigate the potential effect of red photobiomodulation (PBM) as an attractive therapy to downregulate the cytokine storm caused by COVID-19 in a zebrafish model. RT-qPCR analyses and protein-protein interaction prediction among SARS-CoV-2 and  proteins showed that recombinant Spike protein (rSpike) was responsible for generating systemic inflammatory processes with significantly increased levels of pro-inflammatory (, , , and ), oxidative stress () and energy metabolism () mRNA markers, with a pattern similar to those observed in COVID-19 cases in humans. On the other hand, PBM treatment was able to decrease the mRNA levels of these pro-inflammatory and oxidative stress markers compared with rSpike in various tissues, promoting an anti-inflammatory response. Conversely, PBM promotes cellular and tissue repair of injured tissues and significantly increases the survival rate of rSpike-inoculated individuals. Additionally, metabolomics analysis showed that the most-impacted metabolic pathways between PBM and the rSpike treated groups were related to steroid metabolism, immune system, and lipid metabolism. Together, our findings suggest that the inflammatory process is an incisive feature of COVID-19 and red PBM can be used as a novel therapeutic agent for COVID-19 by regulating the inflammatory response. Nevertheless, the need for more clinical trials remains, and there is a significant gap to overcome before clinical trials can commence.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37047078,

title = {Photobiomodulation Reduces the Cytokine Storm Syndrome Associated with COVID-19 in the Zebrafish Model},

author = {Ivana F Rosa and Ana P B Peçanha and Tábata R B Carvalho and Leonardo S Alexandre and Vinícius G Ferreira and Lucas B Doretto and Beatriz M Souza and Rafael T Nakajima and Patrick da Silva and Ana P Barbosa and Leticia Gomes-de-Pontes and Camila G Bomfim and Glaucia M Machado-Santelli and Antonio Condino-Neto and Cristiane R Guzzo and Jean P S Peron and Magaiver Andrade-Silva and Niels O S Câmara and Anali M B Garnique and Renata J Medeiros and Fausto K Ferraris and Leonardo J G Barcellos and Jose D Correia-Junior and Jorge Galindo-Villegas and Mônica F R Machado and Angela Castoldi and Susana L Oliveira and Camila C Costa and Marco A A Belo and Giovane Galdino and Germán G Sgro and Natalia F Bueno and Silas F Eto and Flávio P Veras and Bianca H V Fernandes and Paulo R S Sanches and Eduardo M Cilli and Guilherme Malafaia and Rafael H Nóbrega and Aguinaldo S Garcez and Emanuel Carrilho and Ives Charlie-Silva},

doi = {10.3390/ijms24076104},

issn = {1422-0067},

year  = {2023},

date = {2023-03-01},

urldate = {2023-03-01},

journal = {Int J Mol Sci},

volume = {24},

number = {7},

abstract = {Although the exact mechanism of the pathogenesis of coronavirus SARS-CoV-2 (COVID-19) is not fully understood, oxidative stress and the release of pro-inflammatory cytokines have been highlighted as playing a vital role in the pathogenesis of the disease. In this sense, alternative treatments are needed to reduce the level of inflammation caused by COVID-19. Therefore, this study aimed to investigate the potential effect of red photobiomodulation (PBM) as an attractive therapy to downregulate the cytokine storm caused by COVID-19 in a zebrafish model. RT-qPCR analyses and protein-protein interaction prediction among SARS-CoV-2 and  proteins showed that recombinant Spike protein (rSpike) was responsible for generating systemic inflammatory processes with significantly increased levels of pro-inflammatory (, , , and ), oxidative stress () and energy metabolism () mRNA markers, with a pattern similar to those observed in COVID-19 cases in humans. On the other hand, PBM treatment was able to decrease the mRNA levels of these pro-inflammatory and oxidative stress markers compared with rSpike in various tissues, promoting an anti-inflammatory response. Conversely, PBM promotes cellular and tissue repair of injured tissues and significantly increases the survival rate of rSpike-inoculated individuals. Additionally, metabolomics analysis showed that the most-impacted metabolic pathways between PBM and the rSpike treated groups were related to steroid metabolism, immune system, and lipid metabolism. Together, our findings suggest that the inflammatory process is an incisive feature of COVID-19 and red PBM can be used as a novel therapeutic agent for COVID-19 by regulating the inflammatory response. Nevertheless, the need for more clinical trials remains, and there is a significant gap to overcome before clinical trials can commence.},

keywords = {COVID-19},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36617817b,

title = {Allergy, asthma, and proteomics: opportunities with immediate impact},

author = {Renata Harumi Cruz and Leticia Gomes de Pontes and Antonio Condino-Neto},

doi = {10.15586/aei.v51i1.567},

issn = {1578-1267},

year  = {2023},

date = {2023-01-01},

journal = {Allergol Immunopathol (Madr)},

volume = {51},

number = {1},

pages = {16--21},

abstract = {Allergy is widely discussed by researchers due to its complex mechanism that leads to disorders and injuries, but the reason behind the allergic status remains unclear. Current treatments are insufficient to improve the patient's quality of life significantly. New technologies in scientific and technological development are emerging. For instance, the union between allergy and peptidomics and bioinformatics tools may help fill the gaps in this field, diagnosis, and treatment. In this review, we look at peptidomics and address some findings, such as target proteins or biomarkers that help better understand mechanisms that lead to inflammation, organ damage, and, consequently, poor quality of life or even death.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36617817,

title = {Allergy, asthma, and proteomics: opportunities with immediate impact},

author = {Renata Harumi Cruz and Leticia Gomes de Pontes and Antonio Condino-Neto},

doi = {10.15586/aei.v51i1.567},

issn = {1578-1267},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {Allergol Immunopathol (Madr)},

volume = {51},

number = {1},

pages = {16--21},

abstract = {Allergy is widely discussed by researchers due to its complex mechanism that leads to disorders and injuries, but the reason behind the allergic status remains unclear. Current treatments are insufficient to improve the patient's quality of life significantly. New technologies in scientific and technological development are emerging. For instance, the union between allergy and peptidomics and bioinformatics tools may help fill the gaps in this field, diagnosis, and treatment. In this review, we look at peptidomics and address some findings, such as target proteins or biomarkers that help better understand mechanisms that lead to inflammation, organ damage, and, consequently, poor quality of life or even death.},

keywords = {alergias, asma, genética},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36324795b,

title = {Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19},

author = {Daniela Matuozzo and Estelle Talouarn and Astrid Marchal and Jeremy Manry and Yoann Seeleuthner and Yu Zhang and Alexandre Bolze and Matthieu Chaldebas and Baptiste Milisavljevic and Peng Zhang and Adrian Gervais and Paul Bastard and Takaki Asano and Lucy Bizien and Federica Barzaghi and Hassan Abolhassani and Ahmad Abou Tayoun and Alessandro Aiuti and Ilad Alavi Darazam and Luis M Allende and Rebeca Alonso-Arias and Andrés Augusto Arias and Gokhan Aytekin and Peter Bergman and Simone Bondesan and Yenan T Bryceson and Ingrid G Bustos and Oscar Cabrera-Marante and Sheila Carcel and Paola Carrera and Giorgio Casari and Khalil Chaïbi and Roger Colobran and Antonio Condino-Neto and Laura E Covill and Loubna El Zein and Carlos Flores and Peter K Gregersen and Marta Gut and Filomeen Haerynck and Rabih Halwani and Selda Hancerli and Lennart Hammarström and Nevin Hatipoğlu and Adem Karbuz and Sevgi Keles and Christèle Kyheng and Rafael Leon-Lopez and Jose Luis Franco and Davood Mansouri and Javier Martinez-Picado and Ozge Metin Akcan and Isabelle Migeotte and Pierre-Emmanuel Morange and Guillaume Morelle and Andrea Martin-Nalda and Giuseppe Novelli and Antonio Novelli and Tayfun Ozcelik and Figen Palabiyik and Qiang Pan-Hammarström and Rebeca Pérez de Diego and Laura Planas-Serra and Daniel E Pleguezuelo and Carolina Prando and Aurora Pujol and Luis Felipe Reyes and Jacques G Rivière and Carlos Rodriguez-Gallego and Julian Rojas and Patrizia Rovere-Querini and Agatha Schlüter and Mohammad Shahrooei and Ali Sobh and Pere Soler-Palacin and Yacine Tandjaoui-Lambiotte and Imran Tipu and Cristina Tresoldi and Jesus Troya and Diederik van de Beek and Mayana Zatz and Pawel Zawadzki and Saleh Zaid Al-Muhsen and Hagit Baris-Feldman and Manish J Butte and Stefan N Constantinescu and Megan A Cooper and Clifton L Dalgard and Jacques Fellay and James R Heath and Yu-Lung Lau and Richard P Lifton and Tom Maniatis and Trine H Mogensen and Horst von Bernuth and Alban Lermine and Michel Vidaud and Anne Boland and Jean-François Deleuze and Robert Nussbaum and Amanda Kahn-Kirby and France Mentre and Sarah Tubiana and Guy Gorochov and Florence Tubach and Pierre Hausfater and  and  and  and  and  and  and  and  and  and Isabelle Meyts and Shen-Ying Zhang and Anne Puel and Luigi D Notarangelo and Stephanie Boisson-Dupuis and Helen C Su and Bertrand Boisson and Emmanuelle Jouanguy and Jean-Laurent Casanova and Qian Zhang and Laurent Abel and Aurélie Cobat},

doi = {10.1101/2022.10.22.22281221},

year  = {2022},

date = {2022-10-01},

journal = {medRxiv},

abstract = {BACKGROUND: We previously reported inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity in 1-5% of unvaccinated patients with life-threatening COVID-19, and auto-antibodies against type I IFN in another 15-20% of cases.nnMETHODS: We report here a genome-wide rare variant burden association analysis in 3,269 unvaccinated patients with life-threatening COVID-19 (1,301 previously reported and 1,968 new patients), and 1,373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. A quarter of the patients tested had antibodies against type I IFN (234 of 928) and were excluded from the analysis.nnRESULTS: No gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was  , with an OR of 27.68 (95%CI:1.5-528.7,  1.1×10  ), in analyses restricted to biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70 [95%CI:1.3-8.2],  2.1×10  ). Adding the recently reported  COVID-19 locus strengthened this enrichment, particularly under a recessive model (OR=19.65 [95%CI:2.1-2635.4];  3.4×10  ). When these 14 loci and  were considered, all individuals hemizygous (  =20) or homozygous (  =5) for pLOF or bLOF variants were patients (OR=39.19 [95%CI:5.2-5037.0],  =4.7×10  ), who also showed an enrichment in heterozygous variants (OR=2.36 [95%CI:1.0-5.9],  =0.02). Finally, the patients with pLOF or bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years;  1.68×10  ).nnCONCLUSIONS: Rare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36324795,

title = {Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19},

author = {Daniela Matuozzo and Estelle Talouarn and Astrid Marchal and Jeremy Manry and Yoann Seeleuthner and Yu Zhang and Alexandre Bolze and Matthieu Chaldebas and Baptiste Milisavljevic and Peng Zhang and Adrian Gervais and Paul Bastard and Takaki Asano and Lucy Bizien and Federica Barzaghi and Hassan Abolhassani and Ahmad Abou Tayoun and Alessandro Aiuti and Ilad Alavi Darazam and Luis M Allende and Rebeca Alonso-Arias and Andrés Augusto Arias and Gokhan Aytekin and Peter Bergman and Simone Bondesan and Yenan T Bryceson and Ingrid G Bustos and Oscar Cabrera-Marante and Sheila Carcel and Paola Carrera and Giorgio Casari and Khalil Chaïbi and Roger Colobran and Antonio Condino-Neto and Laura E Covill and Loubna El Zein and Carlos Flores and Peter K Gregersen and Marta Gut and Filomeen Haerynck and Rabih Halwani and Selda Hancerli and Lennart Hammarström and Nevin Hatipoğlu and Adem Karbuz and Sevgi Keles and Christèle Kyheng and Rafael Leon-Lopez and Jose Luis Franco and Davood Mansouri and Javier Martinez-Picado and Ozge Metin Akcan and Isabelle Migeotte and Pierre-Emmanuel Morange and Guillaume Morelle and Andrea Martin-Nalda and Giuseppe Novelli and Antonio Novelli and Tayfun Ozcelik and Figen Palabiyik and Qiang Pan-Hammarström and Rebeca Pérez de Diego and Laura Planas-Serra and Daniel E Pleguezuelo and Carolina Prando and Aurora Pujol and Luis Felipe Reyes and Jacques G Rivière and Carlos Rodriguez-Gallego and Julian Rojas and Patrizia Rovere-Querini and Agatha Schlüter and Mohammad Shahrooei and Ali Sobh and Pere Soler-Palacin and Yacine Tandjaoui-Lambiotte and Imran Tipu and Cristina Tresoldi and Jesus Troya and Diederik van de Beek and Mayana Zatz and Pawel Zawadzki and Saleh Zaid Al-Muhsen and Hagit Baris-Feldman and Manish J Butte and Stefan N Constantinescu and Megan A Cooper and Clifton L Dalgard and Jacques Fellay and James R Heath and Yu-Lung Lau and Richard P Lifton and Tom Maniatis and Trine H Mogensen and Horst von Bernuth and Alban Lermine and Michel Vidaud and Anne Boland and Jean-François Deleuze and Robert Nussbaum and Amanda Kahn-Kirby and France Mentre and Sarah Tubiana and Guy Gorochov and Florence Tubach and Pierre Hausfater and and and and and and and and and and Isabelle Meyts and Shen-Ying Zhang and Anne Puel and Luigi D Notarangelo and Stephanie Boisson-Dupuis and Helen C Su and Bertrand Boisson and Emmanuelle Jouanguy and Jean-Laurent Casanova and Qian Zhang and Laurent Abel and Aurélie Cobat},

doi = {10.1101/2022.10.22.22281221},

year  = {2022},

date = {2022-10-01},

urldate = {2022-10-01},

journal = {medRxiv},

abstract = {BACKGROUND: We previously reported inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity in 1-5% of unvaccinated patients with life-threatening COVID-19, and auto-antibodies against type I IFN in another 15-20% of cases.nnMETHODS: We report here a genome-wide rare variant burden association analysis in 3,269 unvaccinated patients with life-threatening COVID-19 (1,301 previously reported and 1,968 new patients), and 1,373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. A quarter of the patients tested had antibodies against type I IFN (234 of 928) and were excluded from the analysis.nnRESULTS: No gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was  , with an OR of 27.68 (95%CI:1.5-528.7,  1.1×10  ), in analyses restricted to biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70 [95%CI:1.3-8.2],  2.1×10  ). Adding the recently reported  COVID-19 locus strengthened this enrichment, particularly under a recessive model (OR=19.65 [95%CI:2.1-2635.4];  3.4×10  ). When these 14 loci and  were considered, all individuals hemizygous (  =20) or homozygous (  =5) for pLOF or bLOF variants were patients (OR=39.19 [95%CI:5.2-5037.0],  =4.7×10  ), who also showed an enrichment in heterozygous variants (OR=2.36 [95%CI:1.0-5.9],  =0.02). Finally, the patients with pLOF or bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years;  1.68×10  ).nnCONCLUSIONS: Rare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old.},

keywords = {COVID-19},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35503492b,

title = {SCID and Other Inborn Errors of Immunity with Low TRECs - the Brazilian Experience},

author = {Lucila Akune Barreiros and Jusley Lira Sousa and Christoph Geier and Alexander Leiss-Piller and Marilia Pylles Patto Kanegae and Tábata Takahashi França and Bertrand Boisson and Alessandra Miramontes Lima and Beatriz Tavares Costa-Carvalho and Carolina Sanchez Aranda and Maria Isabel de Moraes-Pinto and Gesmar Rodrigues Silva Segundo and Janaira Fernandes Severo Ferreira and Fabíola Scancetti Tavares and Flávia Alice Timburiba de Medeiros Guimarães and Eliana Cristina Toledo and Ana Carolina da Matta Ain and Iramirton Figueirêdo Moreira and Gustavo Soldatelli and Anete Sevciovic Grumach and Mayra de Barros Dorna and Cristina Worm Weber and Regina Sumiko Watanabe Di Gesu and Vera Maria Dantas and Fátima Rodrigues Fernandes and Troy Robert Torgerson and Hans Dietrich Ochs and Jacinta Bustamante and Jolan Eszter Walter and Antonio Condino-Neto},

doi = {10.1007/s10875-022-01275-9},

issn = {1573-2592},

year  = {2022},

date = {2022-08-01},

journal = {J Clin Immunol},

volume = {42},

number = {6},

pages = {1171--1192},

abstract = {Severe combined immunodeficiency, SCID, is a pediatric emergency that represents the most critical group of inborn errors of immunity (IEI). Affected infants present with early onset life-threatening infections due to absent or non-functional T cells. Without early diagnosis and curative treatment, most die in early infancy. As most affected infants appear healthy at birth, newborn screening (NBS) is essential to identify and treat patients before the onset of symptoms. Here, we report 47 Brazilian patients investigated between 2009 and 2020 for SCID due to either a positive family history and/or clinical impression and low TRECs. Based on clinical presentation, laboratory finding, and genetic information, 24 patients were diagnosed as typical SCID, 14 as leaky SCID, and 6 as Omenn syndrome; 2 patients had non-SCID IEI, and 1 remained undefined. Disease onset median age was 2 months, but at the time of diagnosis and treatment, median ages were 6.5 and 11.5 months, respectively, revealing considerable delay which affected negatively treatment success. While overall survival was 51.1%, only 66.7% (30/45) lived long enough to undergo hematopoietic stem-cell transplantation, which was successful in 70% of cases. Forty-three of 47 (91.5%) patients underwent genetic testing, with a 65.1% success rate. Even though our patients did not come from the NBS programs, the diagnosis of SCID improved in Brazil during the pilot programs, likely due to improved medical education. However, we estimate that at least 80% of SCID cases are still missed. NBS-SCID started to be universally implemented in the city of São Paulo in May 2021, and it is our hope that other cities will follow, leading to early diagnosis and higher survival of SCID patients in Brazil.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35503492,

title = {SCID and Other Inborn Errors of Immunity with Low TRECs - the Brazilian Experience},

author = {Lucila Akune Barreiros and Jusley Lira Sousa and Christoph Geier and Alexander Leiss-Piller and Marilia Pylles Patto Kanegae and Tábata Takahashi França and Bertrand Boisson and Alessandra Miramontes Lima and Beatriz Tavares Costa-Carvalho and Carolina Sanchez Aranda and Maria Isabel de Moraes-Pinto and Gesmar Rodrigues Silva Segundo and Janaira Fernandes Severo Ferreira and Fabíola Scancetti Tavares and Flávia Alice Timburiba de Medeiros Guimarães and Eliana Cristina Toledo and Ana Carolina da Matta Ain and Iramirton Figueirêdo Moreira and Gustavo Soldatelli and Anete Sevciovic Grumach and Mayra de Barros Dorna and Cristina Worm Weber and Regina Sumiko Watanabe Di Gesu and Vera Maria Dantas and Fátima Rodrigues Fernandes and Troy Robert Torgerson and Hans Dietrich Ochs and Jacinta Bustamante and Jolan Eszter Walter and Antonio Condino-Neto},

doi = {10.1007/s10875-022-01275-9},

issn = {1573-2592},

year  = {2022},

date = {2022-08-01},

urldate = {2022-08-01},

journal = {J Clin Immunol},

volume = {42},

number = {6},

pages = {1171--1192},

abstract = {Severe combined immunodeficiency, SCID, is a pediatric emergency that represents the most critical group of inborn errors of immunity (IEI). Affected infants present with early onset life-threatening infections due to absent or non-functional T cells. Without early diagnosis and curative treatment, most die in early infancy. As most affected infants appear healthy at birth, newborn screening (NBS) is essential to identify and treat patients before the onset of symptoms. Here, we report 47 Brazilian patients investigated between 2009 and 2020 for SCID due to either a positive family history and/or clinical impression and low TRECs. Based on clinical presentation, laboratory finding, and genetic information, 24 patients were diagnosed as typical SCID, 14 as leaky SCID, and 6 as Omenn syndrome; 2 patients had non-SCID IEI, and 1 remained undefined. Disease onset median age was 2 months, but at the time of diagnosis and treatment, median ages were 6.5 and 11.5 months, respectively, revealing considerable delay which affected negatively treatment success. While overall survival was 51.1%, only 66.7% (30/45) lived long enough to undergo hematopoietic stem-cell transplantation, which was successful in 70% of cases. Forty-three of 47 (91.5%) patients underwent genetic testing, with a 65.1% success rate. Even though our patients did not come from the NBS programs, the diagnosis of SCID improved in Brazil during the pilot programs, likely due to improved medical education. However, we estimate that at least 80% of SCID cases are still missed. NBS-SCID started to be universally implemented in the city of São Paulo in May 2021, and it is our hope that other cities will follow, leading to early diagnosis and higher survival of SCID patients in Brazil.},

keywords = {Erros Inatos da Imunidade, SCID, TRECs/KRECs},

pubstate = {published},

tppubtype = {article}

}