New and future immunomodulatory therapy in type 1 diabetes

被引：32

作者：

Tooley, James E.

Waldron-Lynch, Frank

Herold, Kevan C. ^{[1
]}

机构：

[1] Yale Univ, Dept Immunobiol, New Haven, CT 06511 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2012年 / 18卷 / 03期

基金：

美国国家卫生研究院;

关键词：

type; 1; diabetes; immunotherapy; metabolic therapy; biologies; BETA-CELL FUNCTION; GLUTAMIC-ACID DECARBOXYLASE; PROTEIN PEPTIDE DIAPEP277; ANTI-CD3; MONOCLONAL-ANTIBODY; RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; REGULATORY T-CELLS; PHASE-II TRIAL; NOD MICE; RECENT-ONSET;

D O I：

10.1016/j.molmed.2012.01.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Type 1 diabetes is a common autoimmune disease that affects millions of people worldwide and has an incidence that is increasing at a striking rate, especially in young children. It results from the targeted self-destruction of the insulin-secreting 13 cells of the pancreas and requires lifelong insulin treatment. The effects of chronic hyperglycemia the result of insulin deficiency include secondary endorgan complications. Over the past two decades our increased understanding of the pathogenesis of this disease has led to the development of new immunomodulatory treatments. None have yet received regulatory approval, but this report highlights recent progress in this area.

引用

收藏

页码：173 / 181

页数：9

相关论文

共 79 条

[1] Modulating the Natural History of Type 1 Diabetes in Children at High Genetic Risk by Mucosal Insulin Immunization [J].

Achenbach, Peter ;

Barker, Jennifer ;

Bonifacio, Ezio .

CURRENT DIABETES REPORTS, 2008, 8 (02) :87-93

[2] Clinical evidence for the safety of GAD65 immunomodulation in adult-onset autoimmune diabetes [J].

Agardh, CD ;

Cilio, CM ;

Lethagen, Å ;

Lynch, K ;

Leslie, RDG ;

Palmér, M ;

Harris, RA ;

Robertson, JA ;

Lernmark, Å .

JOURNAL OF DIABETES AND ITS COMPLICATIONS, 2005, 19 (04) :238-246

[3]

ALEGRE ML, 1994, TRANSPLANTATION, V57, P1537

[4] T-cell autoantigens in the non-obese diabetic mouse model of autoimmune diabetes [J].

Babad, Jeffrey ;

Geliebter, Ari ;

DiLorenzo, Teresa P. .

IMMUNOLOGY, 2010, 131 (04) :459-465

[5] IDENTIFICATION OF THE 64K AUTOANTIGEN IN INSULIN-DEPENDENT DIABETES AS THE GABA-SYNTHESIZING ENZYME GLUTAMIC-ACID DECARBOXYLASE [J].

BAEKKESKOV, S ;

AANSTOOT, HJ ;

CHRISTGAU, S ;

REETZ, A ;

SOLIMENA, M ;

CASCALHO, M ;

FOLLI, F ;

RICHTEROLESEN, H ;

CAMILLI, PD .

NATURE, 1990, 347 (6289) :151-156

[6] TGF-β-dependent mechanisms mediate restoration of self-tolerance induced by antibodies to CD3 in overt autoimmune diabetes [J].

Belghith, M ;

Bluestone, JA ;

Barriot, S ;

Mégret, J ;

Bach, JF ;

Chatenoud, L .

NATURE MEDICINE, 2003, 9 (09) :1202-1208

[7] ORAL-ADMINISTRATION OF HUMAN INSULIN TO NOD MICE GENERATES CD4(+) T-CELLS THAT SUPPRESS ADOPTIVE TRANSFER OF DIABETES [J].

BERGEROT, I ;

FABIEN, N ;

MAGUER, V ;

THIVOLET, C .

JOURNAL OF AUTOIMMUNITY, 1994, 7 (05) :655-663

[8]

Bizzarri C, 2010, DIABETES CARE, V33, P1962, DOI [10.2337/dc10-0814, 10.2337/dc10-1168]

[9] Genetics, pathogenesis and clinical interventions in type 1 diabetes [J].

Bluestone, Jeffrey A. ;

Herold, Kevan ;

Eisenbarth, George .

NATURE, 2010, 464 (7293) :1293-1300

[10] LIMITED DURATION OF REMISSION OF INSULIN DEPENDENCY IN CHILDREN WITH RECENT OVERT TYPE-I DIABETES TREATED WITH LOW-DOSE CYCLOSPORINE [J].

BOUGNERES, PF ;

LANDAIS, P ;

BOISSON, C ;

CAREL, JC ;

FRAMENT, N ;

BOITARD, C ;

CHAUSSAIN, JL ;

BACH, JF .

DIABETES, 1990, 39 (10) :1264-1272

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