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Article ; Online: The role of indoleamine 2, 3 dioxygenase in regulating host immunity to leishmania infection.

Makala, Levi H C

2012 Volume 19, Page(s) 5

Abstract: Pathogen persistence in immune-competent hosts represents an immunological paradox. Increasing evidence suggests that some pathogens, such as, Leishmania major (L. major) have evolved strategies and mechanisms that actively suppress host adaptive ... ...

Abstract	Pathogen persistence in immune-competent hosts represents an immunological paradox. Increasing evidence suggests that some pathogens, such as, Leishmania major (L. major) have evolved strategies and mechanisms that actively suppress host adaptive immunity. If this notion is correct conventional vaccination therapies may be ineffective in enhancing host immunity, unless natural processes that suppress host immunity are also targeted therapeutically. The key problem is that the basis of pathogen persistence in immune-competent individuals is unknown, despite decades of intense research. This fact, coupled with poor health care and a dearth of effective treatments means that these diseases will remain a scourge on humans unless a better understanding of why the immune system tolerates such infections emerges from research. Indoleamine 2,3-dioxygenase (IDO) has been shown to act as a molecular switch regulating host responses, and IDO inhibitor drugs shown to possess potential in enhancing host immunity to established leishmania infections. It is hoped that this review will help stimulate and help generate critical new knowledge pertaining to the IDO mechanism and how to exploit it to suppress T cell mediated immunity, thus offer an innovative approach to studying the basis of chronic leishmania infection in mice.
MeSH term(s)	Animals ; Chronic Disease ; Dendritic Cells/immunology ; Disease Models, Animal ; Host-Parasite Interactions ; Humans ; Immunity, Cellular ; Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Leishmania major/immunology ; Leishmaniasis/immunology ; Mice ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Indoleamine-Pyrrole 2,3,-Dioxygenase
Language	English
Publishing date	2012-01-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/1423-0127-19-5
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Article: Dendritic cells: a specialized complex system of antigen presenting cells.

Makala, Levi H C / Nagasawa, Hideyuki

The Journal of veterinary medical science

2002 Volume 64, Issue 3, Page(s) 181–193

Abstract: The dendritic cell (DC) network is a specialized system for presenting antigen to naive or quiescent T cells, and consequently plays a central role in the induction of T cell and B cell immunity in vivo. Despite considerable achievements in the last ten ... ...

Abstract	The dendritic cell (DC) network is a specialized system for presenting antigen to naive or quiescent T cells, and consequently plays a central role in the induction of T cell and B cell immunity in vivo. Despite considerable achievements in the last ten years, in our understanding of how DC induce and regulate immune responses, much remains to be learned about this complex system of cells. The history and current status of DC termed "directors of the immune system orchestra" is reviewed. The present understanding of DC cell biology, function and use, taking into account their complexity is discussed.
MeSH term(s)	Animals ; Antigens, Differentiation/immunology ; Dendritic Cells/enzymology ; Dendritic Cells/immunology ; Dendritic Cells/ultrastructure ; Humans
Chemical Substances	Antigens, Differentiation
Language	English
Publishing date	2002-05-07
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1071753-5
ISSN	1347-7439 ; 0916-7250
ISSN (online)	1347-7439
ISSN	0916-7250
DOI	10.1292/jvms.64.181
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Article: Mentored Training to Increase Diversity among Faculty in the Biomedical Sciences: The NHLBI Summer Institute Programs to Increase Diversity (SIPID) and the Programs to Increase Diversity among Individuals Engaged in Health-related Research (PRIDE).

Rice, Treva K / Jeffe, Donna B / Boyington, Josephine E A / Jobe, Jared B / Dávila-Román, Victor G / Gonzalez, Juan E / Fuentes, Lisa de Las / Makala, Levi H C / Sarkar, Rita / Ogedegbe, Gbenga G / Taylor, Anne L / Czajkowski, Susan / Rao, Dabeeru C / Pace, Betty S / Jean-Louis, Girardin / Boutjdir, Mohamed

Ethnicity & disease

2017 Volume 27, Issue 3, Page(s) 249–256

Abstract: Objective: To report baseline characteristics of junior-level faculty participants in the Summer Institute Programs to Increase Diversity (SIPID) and the Programs to Increase Diversity among individuals engaged in Health-Related Research (PRIDE), which ... ...

Abstract	Objective: To report baseline characteristics of junior-level faculty participants in the Summer Institute Programs to Increase Diversity (SIPID) and the Programs to Increase Diversity among individuals engaged in Health-Related Research (PRIDE), which aim to facilitate participants' career development as independent investigators in heart, lung, blood, and sleep research. Design and setting: Junior faculty from groups underrepresented in the biomedical-research workforce attended two, 2-3 week, annual summer research-education programs at one of six sites. Programs provided didactic and/or laboratory courses, workshops to develop research, writing and career-development skills, as well as a mentoring component, with regular contact maintained via phone, email and webinar conferences. Between summer institutes, trainees participated in a short mid-year meeting and an annual scientific meeting. Participants were surveyed during and after SIPID/PRIDE to evaluate program components. Participants: Junior faculty from underrepresented populations across the United States and Puerto Rico participated in one of three SIPID (2007-2010) or six PRIDE programs (2011-2014). Results: Of 204 SIPID/PRIDE participants, 68% were female; 67% African American and 27% Hispanic/Latino; at enrollment, 75% were assistant professors and 15% instructors, with most (96%) on non-tenure track. Fifty-eight percent had research doctorates (PhD, ScD) and 42% had medical (MD, DO) degrees. Mentees' feedback about the program indicated skills development (eg, manuscript and grant writing), access to networking, and mentoring were the most beneficial elements of SIPID and PRIDE programs. Grant awards shifted from primarily mentored research mechanisms to primarily independent investigator awards after training. Conclusions: Mentees reported their career development benefited from SIPID and PRIDE participation.
MeSH term(s)	Biomedical Research/organization & administration ; Faculty, Medical ; Female ; Humans ; Male ; Mentoring/methods ; Mentors ; National Heart, Lung, and Blood Institute (U.S.) ; Program Development ; United States
Language	English
Publishing date	2017-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1274267-3
ISSN	1945-0826 ; 1049-510X
ISSN (online)	1945-0826
ISSN	1049-510X
DOI	10.18865/ed.27.3.249
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Article: A Perspective on Promoting Diversity in the Biomedical Research Workforce: The National Heart, Lung, and Blood Institute's PRIDE Program.

Boyington, Josephine E A / Maihle, Nita J / Rice, Treva K / Gonzalez, Juan E / Hess, Caryl A / Makala, Levi H / Jeffe, Donna B / Ogedegbe, Gbenga / Rao, Dabeeru C / Dávila-Román, Victor G / Pace, Betty S / Jean-Louis, Girardin / Boutjdir, Mohamed

Ethnicity & disease

2016 Volume 26, Issue 3, Page(s) 379–386

Abstract: Aspiring junior investigators from groups underrepresented in the biomedical sciences face various challenges as they pursue research independence. However, the biomedical research enterprise needs their participation to effectively address critical ... ...

Abstract	Aspiring junior investigators from groups underrepresented in the biomedical sciences face various challenges as they pursue research independence. However, the biomedical research enterprise needs their participation to effectively address critical research issues such as health disparities and health inequities. In this article, we share a research education and mentoring initiative that seeks to address this challenge: Programs to Increase Diversity among Individuals Engaged in Health Related Research (PRIDE), funded by the National Heart, Lung, and Blood Institute (NHLBI). This longitudinal research-education and mentoring program occurs through summer institute programs located at US-based academic institutions. Recruited participants are exposed to didactic and lab-based research-skill enhancement experiences, with year-round mentoring over the course of two years. Mentor-mentee matching is based on shared research interests to promote congruence and to enhance skill acquisition. Program descriptions and sample narratives of participants' perceptions of PRIDE's impact on their career progress are showcased. Additionally, we highlight the overall program design and structure of four of seven funded summer institutes that focus on cardiovascular disease, related conditions, and health disparities. Mentees' testimonials about the value of the PRIDE mentoring approach in facilitating career development are also noted. Meeting the clinical and research needs of an increasingly diverse US population is an issue of national concern. The PRIDE initiative, which focuses on increasing research preparedness and professional development of groups underrepresented in the biomedical research workforce, with an emphasis on mentoring as the critical approach, provides a robust model that is impacting the careers of future investigators.
MeSH term(s)	Biomedical Research ; Career Choice ; Cultural Diversity ; Humans ; Mentors ; National Heart, Lung, and Blood Institute (U.S.) ; Program Development ; Research Personnel ; United States
Language	English
Publishing date	2016-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1274267-3
ISSN	1945-0826 ; 1049-510X
ISSN (online)	1945-0826
ISSN	1049-510X
DOI	10.18865/ed.26.3.379
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Article: Immunology. Antigen-presenting cells in the gut.

Makala, Levi H C / Nishikawa, Yoshifumi / Suzuki, Naoyoshi / Nagasawa, Hideyuki

Journal of biomedical science

2004 Volume 11, Issue 2, Page(s) 130–141

Abstract: It has been known for the past 85 years that mucosal responses can be stimulated by local presentation of antigen and that the gut immune system is capable of mounting both primary and secondary responses to potentially harmful antigens while avoiding ... ...

Abstract	It has been known for the past 85 years that mucosal responses can be stimulated by local presentation of antigen and that the gut immune system is capable of mounting both primary and secondary responses to potentially harmful antigens while avoiding the expression of damaging responses to harmless dietary proteins. How these types of responses are induced and regulated remains unclear. In the gut attention has for some time been focused on Peyer's patches (PP) due to evidence that they play a vital role in the induction of humoral and cellular responses. Moreover, it has been established that MHC class II molecules are found in the gut mucosa on a variety of cell types outside PP, namely the lamina propria (LP). Fed antigens have also been detected in the LP and studies have shown that LP cells can stimulate allogeneic mixed lymphocyte responses and are capable of presenting soluble protein antigen to naïve T cells. This article reviews the present understanding of the possible roles of PP and LP in intestinal immunity in terms of induction, regulation, surveillance of immune responses and the antigen presenting cell types involved.
MeSH term(s)	Animals ; Antigen-Presenting Cells ; CD8-Positive T-Lymphocytes/immunology ; Dendritic Cells/immunology ; Humans ; Intestines/immunology ; Lymphoid Tissue/immunology ; Macrophages/immunology
Language	English
Publishing date	2004-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1159/000076025
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Article ; Online: Type 1 diabetes patients have significantly lower frequency of plasmacytoid dendritic cells in the peripheral blood.

Chen, Xueqin / Makala, Levi H C / Jin, Yulan / Hopkins, Diane / Muir, Andy / Garge, Nikhil / Podolsky, Robert H / She, Jin-Xiong

Clinical immunology (Orlando, Fla.)

2008 Volume 129, Issue 3, Page(s) 413–418

Abstract: Dendritic cells uniquely orchestrate the delicate balance between T cell immunity and regulation and an imbalance favoring immunogenic rather than tolerogenic DC is believed to contribute to the development of autoimmune diseases such as type 1 diabetes ( ...

Abstract	Dendritic cells uniquely orchestrate the delicate balance between T cell immunity and regulation and an imbalance favoring immunogenic rather than tolerogenic DC is believed to contribute to the development of autoimmune diseases such as type 1 diabetes (T1D). In this study, we determined the frequencies of three blood DC subsets (pDC, mDC1 and mDC2) in 72 T1D patients and 75 normal controls using the Miltenyi blood DC enumeration kit. The frequency of blood pDC was found to be negatively correlated with subject age in both normal controls and T1D patients (p=0.0007), while the frequency of mDC1 and mDC2 do not change significantly with subject age. More importantly, the mean frequency of pDC in blood was, after adjusting for age, significantly lower in T1D (mean=0.127%) than controls (mean=0.188%) (p<6.0 x 10(-5)), whereas no difference was observed for mDC1 and mDC2 between T1D and controls. Furthermore, T1D patients have a lower proportion of pDC and higher proportion of mDC1 among the total blood DC population than normal controls. These results indicate that the frequency of blood pDC and the pDC/mDC1 ratio are negatively associated with T1D.
MeSH term(s)	Adolescent ; Adult ; Case-Control Studies ; Cell Count ; Child ; Child, Preschool ; Cohort Studies ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Diabetes Mellitus, Type 1/blood ; Diabetes Mellitus, Type 1/immunology ; Female ; Flow Cytometry ; Humans ; Infant ; Male ; Middle Aged ; Young Adult
Language	English
Publishing date	2008-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2008.08.013
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Article ; Online: Leishmania major attenuates host immunity by stimulating local indoleamine 2,3-dioxygenase expression.

Makala, Levi H C / Baban, Babak / Lemos, Henrique / El-Awady, Ahmed R / Chandler, Phillip R / Hou, De-Yan / Munn, David H / Mellor, Andrew L

The Journal of infectious diseases

2011 Volume 203, Issue 5, Page(s) 715–725

Abstract: Inflammation stimulates immunity but can create immune privilege in some settings. Here, we show that cutaneous Leishmania major infection stimulated expression of the immune regulatory enzyme indoleamine 2,3 dioxygenase (IDO) in local lymph nodes. ... ...

Abstract	Inflammation stimulates immunity but can create immune privilege in some settings. Here, we show that cutaneous Leishmania major infection stimulated expression of the immune regulatory enzyme indoleamine 2,3 dioxygenase (IDO) in local lymph nodes. Induced IDO attenuated the T cell stimulatory functions of dendritic cells and suppressed local T cell responses to exogenous and nominal parasite antigens. IDO ablation reduced local inflammation and parasite burdens, as did pharmacologic inhibition of IDO in mice with established infections. IDO ablation also enhanced local expression of proinflammatory cytokines and induced some CD4(+) T cells to express interleukin (IL) 17. These findings showed that IDO induced by L. major infection attenuated innate and adaptive immune responses. Thus, IDO acts as a molecular switch regulating host responses, and IDO inhibitor drugs are a potential new approach to enhance host immunity to established leishmania infections.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes ; Cytokines/drug effects ; Disease Models, Animal ; Host-Parasite Interactions ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Interleukins ; Leishmania major/enzymology ; Leishmania major/immunology ; Leishmaniasis, Cutaneous/drug therapy ; Leishmaniasis, Cutaneous/parasitology ; Lymph Nodes/enzymology ; Lymph Nodes/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Specific Pathogen-Free Organisms ; T-Lymphocyte Subsets
Chemical Substances	Cytokines ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Interleukins
Language	English
Publishing date	2011-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiq095
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Article ; Online: APC dysfunction is correlated with defective suppression of T cell proliferation in human type 1 diabetes.

Jin, Yulan / Chen, Xueqin / Podolsky, Robert / Hopkins, Diane / Makala, Levi H C / Muir, Andy / She, Jin-Xiong

Clinical immunology (Orlando, Fla.)

2008 Volume 130, Issue 3, Page(s) 272–279

Abstract: It is widely believed that CD4(+)CD25(+) regulatory T cells (Treg) are defective in type 1 diabetes (T1D) and other autoimmune diseases. However, this conclusion is based on the suboptimal in vitro suppression results from very small numbers of subjects. ...

Abstract	It is widely believed that CD4(+)CD25(+) regulatory T cells (Treg) are defective in type 1 diabetes (T1D) and other autoimmune diseases. However, this conclusion is based on the suboptimal in vitro suppression results from very small numbers of subjects. Furthermore, the cells responsible for the suboptimal suppression have not been defined. Therefore, we carried out extensive in vitro suppression assays using both autologous and heterologous donors of Tregs, effector T cells and antigen-presenting cells (APC) from both T1D patients and normal controls. Our in vitro suppression data indicated that a significantly higher proportion (40.0%) of T1D patients have "very low suppression" activity (defined as<25%) by autologous Treg compared to controls (6.3%) (p=0.002). Meta-analysis of the published results confirmed this observation with 45.7% low suppressors in T1D and 7.8% in controls (p=0.00002). Interestingly, suppression assays using heterologous Tregs, effector T cells and APC suggest that the source of APC is correlated with the suppression activity. The frequencies of CD4(+)CD25(+) and CD4(+)CD25(hi) T cells were found to increase with age in normal controls but not in T1D patients, resulting in significantly higher frequencies of CD4(+)CD25(+) (p=0.001) and CD4(+)CD25(hi) (p=0.009) T cells in young T1D subjects than age-matched controls but slightly lower CD4(+)CD25(+) (p=0.003) and CD4(+)CD25(hi) (p=0.08) T cells in old T1D subjects than age-matched controls.
MeSH term(s)	Adolescent ; Adult ; Antigen-Presenting Cells/cytology ; Antigen-Presenting Cells/immunology ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/immunology ; Cell Proliferation ; Cells, Cultured ; Child ; Child, Preschool ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/physiopathology ; Female ; Humans ; Infant ; Interleukin-2 Receptor alpha Subunit/immunology ; Lymphocyte Activation ; Male ; Middle Aged ; Young Adult
Chemical Substances	Interleukin-2 Receptor alpha Subunit
Language	English
Publishing date	2008-11-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2008.10.005
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Article: Immunology

Makala, Levi H.C. / Nishikawa, Yoshifumi / Suzuki, Naoyoshi / Nagasawa, Hideyuki

Journal of Biomedical Science

2004 Volume 11, Issue 2, Page(s) 130–141

Institution	National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-Cho, Obihiro, Japan
Abstract	It has been known for the past 85 years that mucosal responses can be stimulated by local presentation of antigen and that the gut immune system is capable of mounting both primary and secondary responses to potentially harmful antigens while avoiding the expression of damaging responses to harmless dietary proteins. How these types of responses are induced and regulated remains unclear. In the gut attention has for some time been focused on Peyer’s patches (PP) due to evidence that they play a vital role in the induction of humoral and cellular responses. Moreover, it has been established that MHC class II molecules are found in the gut mucosa on a variety of cell types outside PP, namely the lamina propria (LP). Fed antigens have also been detected in the LP and studies have shown that LP cells can stimulate allogeneic mixed lymphocyte responses and are capable of presenting soluble protein antigen to naïve T cells. This article reviews the present understanding of the possible roles of PP and LP in intestinal immunity in terms of induction, regulation, surveillance of immune responses and the antigen presenting cell types involved.
Keywords	Antigen-presenting cell ; Gut ; Lamina propria ; Peyer’s patch ; Mouse
Language	English
Publishing date	2004-02-19
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1159/000076025
Database	Karger publisher's database

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Article ; Online: UFBP1, a Key Component of the Ufm1 Conjugation System, Is Essential for Ufmylation-Mediated Regulation of Erythroid Development.

Cai, Yafei / Pi, Wenhu / Sivaprakasam, Satish / Zhu, Xiaobin / Zhang, Mingsheng / Chen, Jijun / Makala, Levi / Lu, Chunwan / Wu, Jianchu / Teng, Yong / Pace, Betty / Tuan, Dorothy / Singh, Nagendra / Li, Honglin

PLoS genetics

2015 Volume 11, Issue 11, Page(s) e1005643

Abstract: The Ufm1 conjugation system is an ubiquitin-like modification system that consists of Ufm1, Uba5 (E1), Ufc1 (E2), and less defined E3 ligase(s) and targets. The biological importance of this system is highlighted by its essential role in embryogenesis ... ...

Abstract	The Ufm1 conjugation system is an ubiquitin-like modification system that consists of Ufm1, Uba5 (E1), Ufc1 (E2), and less defined E3 ligase(s) and targets. The biological importance of this system is highlighted by its essential role in embryogenesis and erythroid development, but the underlying mechanism is poorly understood. UFBP1 (Ufm1 binding protein 1, also known as DDRGK1, Dashurin and C20orf116) is a putative Ufm1 target, yet its exact physiological function and impact of its ufmylation remain largely undefined. In this study, we report that UFBP1 is indispensable for embryonic development and hematopoiesis. While germ-line deletion of UFBP1 caused defective erythroid development and embryonic lethality, somatic ablation of UFBP1 impaired adult hematopoiesis, resulting in pancytopenia and animal death. At the cellular level, UFBP1 deficiency led to elevated ER (endoplasmic reticulum) stress and activation of unfolded protein response (UPR), and consequently cell death of hematopoietic stem/progenitor cells. In addition, loss of UFBP1 suppressed expression of erythroid transcription factors GATA-1 and KLF1 and blocked erythroid differentiation from CFU-Es (colony forming unit-erythroid) to proerythroblasts. Interestingly, depletion of Uba5, a Ufm1 E1 enzyme, also caused elevation of ER stress and under-expression of erythroid transcription factors in erythroleukemia K562 cells. By contrast, knockdown of ASC1, a newly identified Ufm1 target that functions as a transcriptional co-activator of hormone receptors, led to down-regulation of erythroid transcription factors, but did not elevate basal ER stress. Furthermore, we found that ASC1 was associated with the promoters of GATA-1 and Klf1 in a UFBP1-dependent manner. Taken together, our findings suggest that UFBP1, along with ASC1 and other ufmylation components, play pleiotropic roles in regulation of hematopoietic cell survival and differentiation via modulating ER homeostasis and erythroid lineage-specific gene expression. Modulating the activity of this novel ubiquitin-like system may represent a novel approach to treat blood-related diseases such as anemia.
MeSH term(s)	Animals ; Carrier Proteins/genetics ; Carrier Proteins/physiology ; Embryonic Development ; Erythropoiesis ; Mice ; Mice, Knockout
Chemical Substances	Carrier Proteins ; UFM1-binding protein 1 containing a PCI domain, mouse
Language	English
Publishing date	2015-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1005643
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