MEDICAL GENOMICS GROUP
COMPARATIVE GENOMICS CENTRE

Mail Address: Comparative Genomics Centre,
Molecular Sciences Bldg 21, James Cook University,
Townsville, 4811, Queensland, Australia
Telephone: 61-7-4781 6265 Fax:  61-7-4781 6078


 

RESEARCH REPORT 2011

CONTENTS:

CONTRIBUTIONS TO GENOMICS RESEARCH:

Laboratory Registration Code: Bax

Genes mapped (mouse):
 
Phenotype Locus Name Location Note
Diabetes Idd11 Insulin-dependent diabetes locus 11 4 1

Idd12 Insulin-dependent diabetes locus 12 14 1
Gastritis Gasa1 Gastritis type A locus 1 4 2

Gasa2 Gastritis type A locus 2 4 2

Gasa3 Gastritis type A locus 3 6 3

Gasa4 Gastritis type A locus 4 17 3
Lupus Bana1 BCG-induced antinuclear antibodies locus 1 17 4

Bana2 BCG-induced antinuclear antibodies locus 2 10 4

Bana3 BCG-induced antinuclear antibodies locus 3 1 4

Bah1 BCG-induced autoimmune haemolysis locus 1 17 4

Bah2 BCG-induced autoimmune haemolysis locus 2 16 4

Babs1 BCG-induced autoantibodies locus1 17 4

Babs2 BCG-induced autoantibodies locus2 1 4
NKT cell number Nkt1 Thymic NKT cell number locus 1  1 5

Nkt2 Thymic NKT cell number locus 2 2 5

Notes:

1 Morahan et al (1994) Proc Natl Acad Sci USA 91: 5898-5902
2 Silveira et al (1999) J Immunol 162: 5106-5111.
3 Silveira et al (2001) Immunogenetics 53: 741-750.
4 Jordan et al (2000) J Immunol 165: 1673-1684
5 Esteban et al (2003) J Immunol 171: 2873-2878.

Congenic Mice Generated:
NOD.H2d
NOD.Hc
NOD.Nkrp1b


TYPE 1 DIABETES:

Identification of Genes Controlling Numbers of NKT Cells in NOD Mice
AG Baxter, MA Jordan, JM Fletcher in collaboration with Prof DI Godfrey at Department of Microbiology and Immunology, University of Melboune.

Type 1 diabetes is caused by autoimmune destruction of the insulin-producing islets in the pancreas. NOD mice spontaneously develop type 1 diabetes following autoimmune destruction of the insulin producing beta cells of the pancreas in a manner which is largely dependent on the production of the Th1 associated cytokines IL-2 and IFN-g, and may be inhibited by the Th2 associated cytokines IL-4 and IL-10.

We have identified a deficiency in NOD mice in the numbers of immunoregulatory invariant NKT cells, which  play a critical role in controlling the strength and character of adaptive immune responses. The critical role of this deficiency has been demonstrated by us in adoptive transfer experiments in which a single injection of syngeneic or semiallogeneic thymocyte subpopulations enriched for NKT cells prevented the onset of type 1 diabetes in an IL-4 dependent manner. Genetic control of thymic NKT cell numbers was mapped to two linkage regions: Nkt1 on distal chromosome 1 and Nkt2 on chromosome 2. A NOD.Nkrp1(b).Nkt1(b) congenic mouse strain was developed and characetrised, and microarray expression analyses applied to limit candidate genes within the 95% confidence region. This approach identified Slamf1 (encoding signaling lymphocyte activation molecule) and Slamf6 (encoding Ly108) as potential candidates, and demonstrate retarded signaling lymphocyte activation molecule expression during T cell development of NOD mice, resulting in reduced expression at the CD4(+)CD8(+) stage, which is consistent with decreased NKT cell production and deranged tolerance induction in NOD mice.

Subcongenic mouse strains and Slamf1 transgenic lines were then developed. The long isoform of the C57BL/6 allele of Slamf1 was transgenically expressed on CD4(+)CD8(+) thymocytes under control of an hCD2 minigene. NOD.Nkrp1b.Tg(Slamf1)1 mice, which had a 2-fold increase in SLAM protein expression on CD4(+)CD8(+) thymocytes, had a 2-fold increase in numbers of thymic NKT cells. The additional thymic NKT cells in NOD.Nkrp1b.Tg(Slamf1)1 mice were relatively immature, with a similar subset distribution to those of congenic NOD.Nkrp1b.Nkt1 and NOD.Nkrp1b.Slamf1 mice, which also express increased levels of SLAM on CD4(+)CD8(+) thymocytes and produce larger numbers of NKT cells. Transgenic enhancement of SLAM expression also increased IL-4 and IL-17 production in response to TCR-mediated stimulation. Paradoxically, NOD.Nkrp1b.Tg(Slamf1)2 mice, which had a 7-fold increase in SLAM expression, showed no significant increase in NKT cells numbers; on the contrary, at high transgene copy number, SLAM expression levels correlated inversely with NKT cell numbers, consistent with a contribution to negative selection. These data confirm a role for SLAM in controlling NKT cell development and are consistent with a role in both positive and negative thymic selection of NKT cells.

This project was funded by the National Health and Medical Research Council of Australia, and the Faculty of Medicine, Health and Molecular Sciences.

Publications:

Gene/Environment Interactions in Autoimmune Disease
AG Baxter, JM Fletcher, N Fraser in collaboration with Prof P Brennan at the Colorado State University and Dr Grant Morahan, Walter and Eliza Hall Institute, Melboune.

As a generalisation, people who are heavily exposed to microorganisms are at a low risk of Type 1 diabetes. In an attempt to determine the mechanism by which exposure to mycobacteria can prevent type 1 diabetes, we have tested subfractions of Mycobacterium bovis for their ability to prevent diabetes. A single molecular species, mycolylarabinogalactanpeptidoglycan was responsible for the majority of the protective activity. In addition to this, we are applying two other tools to address this issue. The first is a paired set of M.bovis isolates, one of which prevents diabetes, the other of which does not; the second is a congenic mouse line, NOD.Lsh, which is not protected from diabetes by M.bovis.

In an alternative approach, we have studied the immunological effects on the body of a new vaccine platform, termed "Transcutaneous Immunisation". This system applies skin patch technology to provide "needle free vaccines". Our work has identified one component of this system, the adjuvant used to increase the strength of immune responses to the vaccine, as having the effect of exacerbating ongoing inflammation, namely, islet destruction associated with type 1 diabetes and myelin damage associated with a model of multiple sclerosis. The mechanism of this action appear to be via enhancement of cytokine production.

Publications:
Patent coverage entitled "Mycobacterium cell wall compositions" has been granted in Australia (726734) Canada (2271468) and Europe (97911956.7.) and is pending in USA (09/308192), based on Provisional Patent Application N. PO3593/96 and PCT/AU97/00770.

Baxter AG. (2001) Modelling the effects of genetic and environmental factors on the risk of autoimmune disease. J Autoimmunity 16: 331-335.





MULTIPLE SCLEROSIS:

Role for MyD88, TLR2 and TLR9, but not TLR1, TLR4 or TLR6 in Experimental Autoimmune Encephalomyelitis
AG Baxter, S Miranda-Hernandez, N Gerlach, JM Fletcher, E Biros and H Körner in collaboration with M Mack, Regensburg University Medical Center, Regensburg, Germany.

The potential roles of Toll-like receptors in the etiology and pathogenesis of autoimmune central nervous system inflammation remain contentious. Here, we examined the effects of targeted deletions of TLR1, TLR2, TLR4, TLR6, TLR9 and MyD88 on the induction of MOG35-55 peptide/complete Freund's adjuvant/pertussis toxin-induced autoimmune encephalomyelitis. While C57BL/6.Tlr1-/-, C57BL/6.Tlr4-/- and C57BL/6.Tlr6-/- mice showed normal susceptibility to disease, disease was ameliorated in female C57BL/6.Tlr2-/- and C57BL/6.Tlr9-/- mice and C57BL/6.TLR2/9-/- mice of both sexes. C57BL/6.Myd88-/- mice were completely protected. Lower clinical scores were associated with reduced leukocyte infiltrates. These results were confirmed by passive adoptive transfer of disease into female C57BL/6.Tlr2-/- and C57BL/6.Tlr9-/- mice, where protection in the absence of TLR2 was associated with fewer infiltrating CD4+ cells in the central nervous system (CNS), reduced prevalence of detectable circulating IL6, and increased proportions of central (CD62L+) CD4+CD25+FoxP3+ Treg. These results provide a potential molecular mechanism for the observed effects of TLR signaling on the severity of autoimmune central nervous system inflammation.

Publications:
Baxter AG. The origin and application of experimental autoimmune encephalomyelitis. Nat Rev Immunol. 2007 Nov;7(11):904-12.

Miranda-Hernandez S, Gerlach N, Fletcher JM, Biros E, Mack M, Körner H  and Baxter AG. (2011) Role for MyD88, TLR2 and TLR9, but not TLR1, TLR4 or TLR6 in Experimental Autoimmune Encephalomyelitis in a Controlled Environment. J Immunol 187: 791-804


SYSTEMIC LUPUS ERYTHEMATOSUS:

Effects of BCG and its Subfractions on Autoimmunity in NOD Mice
AG Baxter, and C Hawke in collaboration with Prof P Brennan at the Colorado State University and Ms RR van Driel at the IATIA Group.
 

NOD mice can be protected from Type 1 Diabetes by injection with BCG, which is the vaccine for tuberculosis and leprosy. Intravenous injection of killed BCG vaccine not only prevents diabetes, but also precipitates another autoimmune disease similar to systemic lupus erythematosus (SLE). This syndrome was characterized by haemolytic anaemia, anti-dsDNA and anti-Sm antinuclear autoantibodies, and increased severity of sialadenitis and lupus nephritis. The pattern of nephritis was studied by electron and immunochemical histology and was found to strongly resemble the pathology seen in human lupus nephritis, included mesangiopathic, mesangiocapillary and membranous subclasses of nephritis, and was associated with glomerular immune complex deposition.

The activity of subfractions of lysates of killed BCG is being tested by intravenous injection into NOD mice. One fraction has been identified which prevents diabetes without inducing lupus and the activity of this fraction has been titrated. The activity of the fraction is contained within a single complex molecule. Future work will be directed at determining which (if any) of its subdomains are responsible for its clinical efficacy.

Publications:
Hawke CG, Painter DM, Kirwan PD, van Driel IR, Baxter AG. (2003) Mycobacteria, an environmental enhancer of lupus nephritis in a mouse model of systemic lupus erythematosus. Immunology 208: 70-78
 

Genetics of BCG Induced Lupus in NOD Mice
M Jordan, P Silveira, DP Shepherd, C Chu, SJ Kinder, J Chen, LJ Palmisano, LD Poulton and AG Baxter in collaboration with Dr E Wakeland at the University of Florida, USA.

NOD mice can be protected from Type 1 Diabetes by intravenous injection of killed BCG vaccine. This treatment not only prevents diabetes, but also precipitates another autoimmune disease, lupus. Lupus (or systemic lupus erythematosus, SLE) in these mice is characterized by haemolytic anaemia and the production of autoantibodies which are directed against multiple components of the body, especially the intranuclear antigens double stranded DNA and the Smith (Sm) antigen. These antibodies then form immune complexes with their target antigens in the filtering units of the kidney, the glomeruli, and result in kidney damage. BALB/c mice and B6 mice do not develop lupus after injection with BCG, nor do hybrid mice produced by mating either of these strains with NOD mice.

Systemic lupus erythematosus (SLE) induced by M.bovis in diabetes-prone NOD mice was mapped in a backcross to the BALB/c strain. The subphenotypes - haemolytic anaemia (HA), antinuclear antibodies (ANA) and glomerular immune complex deposition - did not cosegregate, and linkage analysis for each trait was performed independently. HA mapped to two loci: Bah1 at the MHC on chromosome 17, and Bah2 on distal chromosome 16. ANA mapped to three loci: Bana1 at the MHC on chromosome 17, Bana2 on chromosome 10, and Bana3 on distal chromosome 1. Glomerular immune complex deposition did not show significant linkage to any genomic region. Mapping of autoantibodies (Coombs’ or ANA) identified two loci: Babs1 at the MHC, and Babs2 on distal chromosome 1. It has previously been reported that genes conferring susceptibility to different autoimmune diseases map non-randomly to defined regions of the genome. One possible explanation for this clustering is that some alleles at loci within these regions confer susceptibility to multiple autoimmune diseases - the "common gene" hypothesis. With the exception of the H2, this study failed to provide direct support for the common gene hypothesis, since the loci identified as conferring susceptibility to SLE did not colocalise with those previously implicated in diabetes. Three of the four regions identified had, however, been previously implicated in other autoimmune diseases.

This project was funded by the National Health and Medical Research Council of Australia.

Publications:
MA Jordan, PA Silveira, DP Shepherd, C Chu, SJ Kinder, J Chen, LJ Palmisano, AG Baxter. (2000) Linkage analysis of systemic lupus erythematosus induced in diabetes-prone NOD mice by Mycobacterium bovis. J Immunol 165: 1673-1684.

Silveira PA, Baxter AG. (2001) The NOD mouse as a model of SLE. Autoimmunity, 34: 53-64

Hawke CG, Painter DM, Kirwan PD, van Driel IR, Baxter AG. (2003) Mycobacteria, an environmental enhancer of lupus nephritis in a mouse model of systemic lupus erythematosus. Immunology 208: 70-78


TYPE A GASTRITIS:

Genetics of Gastritis
AG Baxter, C Hawke and P Silveira in collaboration with Dr I van Driel and Wendy Cain at the University of Melbourne.

 BALB/c mice, but not B6 mice, develop autoimmune gastritis following removal of the thymus gland on the third day of life. The F1 progeny of BALB/c and B6 mice also develop disease and this tendency is genetically controlled. An F2 cross was performed by mating F1 mice and the genes controlling the expression of gastritis were being mapped by examining the genes of both affected and unaffected mice at multiple loci. A high-resolution scan has been completed and two loci were identified on distal chromosome 4, named Gasa1 and Gasa2.
    Partitioned c2 analysis was used in order to develop a better understanding of the genotypes contributing to susceptibility and resistance at each of these linkage region. This approach revealed that linkage of Gasa1 and Gasa2 to gastritis was due to codominant and recessive BALB/cCrSlc alleles respectively. To identify additional gastritis susceptibility genes, separate linkage studies were performed on Gasa1 heterozygotes and Gasa2 C57BL/6 homozygotes plus heterozygotes so as to minimise the effects of these disease genes. The enhanced sensitivity of these analyses confirmed the existence of a third gastritis susceptibility gene (designated Gasa3) on Chromosome 6. Epistatic interactions between the Gasa2 gastritis susceptibility gene and the H2 were also identified, and the presence of an H2 linked susceptibility gene (Gasa4) confirmed by analysis of H2 congenic mice. The major focus of the project in the future will be to identify the coding sequence of Gasa1 to determine the mechanism by which it causes gastritis.

This project was funded by the National Health and Medical Research Council of Australia.

Publications:
PA Silveira, AG Baxter, W Cain, IR van Driel. (1999) A single major gene controls susceptibility to a neonatal thymectomy induced autoimmune disease. J Immunol  162: 5106-5111.

Silveira PA, Wilson WE, Jordan MA, van Driel IR, Baxter AG. (2001) Identification of the Gasa3 and Gasa4 autoimmune gastritis susceptibility genes using congenic mice and partitioned, segregative and interaction analyses. Immunogenetics 53:741?750.

van Driel IR, Baxter AG, Laurie KL, Zwar TD, La Gruta1 NL, Judd LM, Scarff KL, Siveira PA, and Gleeson PA. (2002) Immunopathogenesis, loss of T cell tolerance and genetics of autoimmune gastritis. Autoimmunity Reviews 1: 290-297.

Baune BT, Dannlowski U, Janssen DAG, Jordan MA, Ohrmann P, Bauer J, Domschke K, Arolt V, Kugel H, Baxter AG, Suslow T. (2010) The IL1B gene is associated with failure to achieve remission and impaired emotion processing in major depression. Biol Psychiatry. 67(6):543-9. [0 (IF = 8.926)]

Jordan MA, Baxter AG. (2008) The genetics of immunoregulatory T cells. J Autoimmun 31:237-244. [24 (IF = 7.231 )]

Allen S, Turner S, Bourges D, Gleeson PA and van Driel IR (2011) Shaping the T cell repertoire in the periphery. Immunol Cell Biol, 89(1), 60-9.

Nguyen N, Judd LM, Kalantzis A, Giraud AS, van Driel IR (2010) Random mutagenesis of the mouse genome: A strategy for discovering gene function and the molecular basis of disease. Am J Physiol. 300(1),1-11.


RECENT PUBLICATIONS

Baxter AG. (2000) Symptomless infection with Ebola virus. Lancet 355:2178-2179 (Invited commentary). [5 (IF = 30.758)]

Baxter AG. (2000) The cells that knew too much. J Clin Invest  105: 1675-1677. (Invited commentary). [3 (IF = 15.387)]

Jordan MA, Silveira PA, Shepherd DP, Chu C, Kinder SJ, ChenJ, Palmisano LJ, Baxter AG. (2000) Linkage analysis of systemic lupus erythematosus induced in diabetes-prone NOD mice by Mycobacterium bovis. J Immunol 165: 1673-1684. [28 (IF = 5.646)]

Godfrey DI, Hammond KJL, Poulton LD, Baxter AG. (2000) NKT cell facts, functions and fallacies. Immunology Today * 21: 573-583 (Commissioned review; Peer reviewed). [536 (IF = 8.768)] * = Retitled Trends in Immunology

Silveira PA, Baxter AG. (2001) The NOD mouse as a model of SLE. Autoimmunity, 34: 53-64 (Peer reviewed). [35 (IF = 2.813)]

 Baxter AG. (2001) Modeling the effects of genetic and environmental factors on the risk of autoimmune disease. J Autoimmunity16: 331-335. (Invited review). [7 (IF = 7.231)]

Poulton LD, Smyth MJ, Hawke C,  Naidenko OV, Silveira P, Shepherd D, Godfrey DI, Baxter AG. (2001) Cytometric and functional analyses of NK and NKT cell deficiencies in NOD mice. Int Immunol 13: 887-896. [90 (IF = 3.403)]

Silveira PA, Wilson WE, Jordan MA, van Driel IR, Baxter AG. (2001) Identification of the Gasa3 and Gasa4 autoimmune gastritis susceptibility genes using congenic mice and partitioned, segregative and interaction analyses. Immunogenetics 53:741–750. [12 (IF = 2.988)]

Hammond KJL, Pellicci DG, Poulton LD, Naidenko OV, Baxter AG, Godfrey DI. (2001) CD1d-restricted NKT cells: an interstrain comparison. J Immunol 167: 1164-1173. [134 (IF = 5.646)]

Sze DMY, Giesajtis G, Brown RD, Raitakari M, Gibson J, Ho J, Baxter AG, Fazekas de St Groth B, BastenA, Joshua DE. (2001) Clonal cytotoxic T cells are expanded in myeloma and reside in the CD8+CD57+CD28- compartment. Blood 98 (9): 2817-2827. [67 (IF = 10.555)]

Poulton LD, Baxter AG (2001) Clinical application of NKT cell assays to the prediction of type 1 diabetes. Diabetes-Metabolism Research and Reviews 17: 429-435 (Commissioned review; peer reviewed). [9 (IF = 2.762)]

Baxter AG (2001)  Louis Pasteur’s beer of revenge. Nature Reviews Immunology 1: 229 -232 (Invited 'Science in Society' submission, peer reviewed). [7 (IF = 32.245)]

Esteban LM, Baxter AG (2001) Polyspecificty of autoimmune responses in type 1 (autoimmune) diabetes. Clin and Exp Immunol 126(2):184-186 (Invited commentary; peer reviewed). [7 (IF = 3.009)]

Baxter AG, Smyth MJ (2002) The role of NK cells in autoimmune disease. Autoimmunity 35: 1-14. (Peer reviewed). [49 (IF = 2.813)]

Baxter AG , Hodgkin PD. (2002) Activation Rules: The two-signal theories of immune activation. Nature Reviews Immunology 2: 439-446 ('Timeline' submisson, peer reviewed). [43 (IF = 32.245)]

Pellicci DG, Hammond KJL., Uldrich A.P., Baxter AG, Smyth MJ, Godfrey DI. (2002). A natural killer T (NKT) cell developmental pathway involving a thymus dependent, NK1.1-CD4+ CD1d-dependent precursor stage. J. Exp Med 195: 835-844. [179 (14.505)]

van Driel IR, Baxter AG, Laurie KL, Zwar TD, La Gruta1 NL, Judd LM, Scarff KL, Siveira PA, and Gleeson PA. (2002) Immunopathogenesis, loss of T cell tolerance and genetics of autoimmune gastritis. Autoimmunity Reviews 1: 290-297. (Peer reviewed). [21 (IF = 6.368)]

Hawke CG, Painter DM, Kirwan PD, van Driel IR, Baxter AG. (2003) Mycobacteria, an environmental enhancer of lupus nephritis in a mouse model of systemic lupus erythematosus. Immunology 208: 70-78 [5 (IF = 3.276)]

Esteban LM, Tsoutsman T, Jordan MA, Roach D, Poulton LD, Brooks A, Naidenko OV, Sidobre S,  Godfrey DI, Baxter AG. (2003) Genetic control of NKT cell numbers maps to major diabetes and lupus loci. J Immunol 171: 2873-2878. [47 (IF = 5.646)]

Crowe NY, Godfrey DI, Baxter AG. (2003) Natural killer T cells are targets for HIV infection. Immunology 108:1-2.(Invited commentary) [0 (IF = 3.276)]

Smallwood L, Baxter AG. (2004) On lawnmowers and lay-down misères. Immunology 111: 252-253 (Invited commentary) [1 (IF = 3.276)]

Riminton DS, Kandasamy R, Dravec D, Basten A, Baxter AG. (2004) Dermal enhancement: bacterial products on intact skin induce and augment organ-specific autoimmune disease. J Immunol 174:302-309. [10 (IF = 5.646)]

Berzins SP, Kyparissoudis K, Pellicci DG, Hammond KJ, Sidobre S, Baxter AG, Smyth MJ, Kronenberg M, Godfrey DI. (2004) Systemic NKT cell deficiency in NOD mice is not detected in peripheral blood: implications for human studies. Immunol Cell Biol. 82(3):247-52. [23 (IF = 4.2)]

Liston A, Lesage S, Gray DHD, O’Reilly LA, Strasser A, Fahrer AM, Boyd RL, Wilson J, Baxter AG, Gallo EM, Crabtree GR, Peng K, Wilson SR, Goodnow CG. (2004) Generalised resistance to thymic deletion in the NOD mouse: a polygenic trait characterized by defective induction of Bim. Immunity 21: 817-30. [75 (IF = 20.589)]

Jordan MA, Fletcher J and Baxter AG. (2004) Genetic Control of NKT Cell Numbers. Immunol Cell Biol 82:276-84. (Commissioned review) [13 (IF = 4.2)]

Fletcher JM, Jordan MA, Baxter AG. (2004) Type 1 diabetes and NKT cells: a report on the 3rd international workshop on NKT cells and CD1-mediated antigen presentation. Review of Diabetic Studies 1: 139-141. [journal not indexed]

Baxter AG, Duckworth RC. (2004) Models of type 1 (autoimmune) diabetes. Drug discovery today: disease models 1: 451-455 (Commissioned review, Peer reviewed). [1 (IF = 4.94)]

Baxter AG, Silveira PA, Wilson WE, Jordan MA and van Driel IR. (2005) Genetic control of susceptibility to autoimmune gastritis. Int Rev Immunol 24: 55-62 (Peer reviewed) [6 (IF = 2.641)]

Biros E, Jordan MA, Baxter AG. (2005) Genes mediating environment interactions in type 1 diabetes. Review of Diabetic Studies 2: 192-207 [journal not indexed]

 Jordan MA, Fletcher JM, Pellicci D, Baxter AG. (2007) Slamf1 the NKT Cell Control Gene Nkt1. J Immunol 178:1618-1627. [36 (IF = 5.646)]

Grose RH, Thompson FM, Baxter AG, Pellicci DG, Cummins AG. (2007) Deficiency of invariant NK T cells in Crohn's disease and ulcerative colitis. Dig Dis Sci.  52:1415-22. [13 (IF = 1.838)]

Ang DKY, Brodnicki TC, Wilson WE, Gliddon BE, Jordan MA, Baxter AG#, van Driel IR#. (2007) Two genetic loci independently confer susceptibility to autoimmune gastritis. Int Immunol 19(9):1135-44. (# = authors contributed equally) [2 (IF = 3.403)]

Hodgkin PD, Heath WR, Baxter AG. (2007) The Clonal Selection Theory: 50 Years Since the Revolution. Nat Immunol 8:1019-1026. [10 (IF = 26 )]

Baxter AG. (2007) The origin and application of experimental autoimmune encephalomyelitis. Nat Rev Immunol 7: 904-12. [89 (IF = 32.245 )]

Jordan MA, Baxter AG. (2008) Quantitative and Qualitative approaches to GOD: the first 10 years of the clonal selection theory. Immunol Cell Biol 86: 72-79. [3 (IF = 4.2)]
 
Jordan MA, Baxter AG. (2008) The genetics of immunoregulatory T cells. J Autoimmun 31:237-244. [24 (IF = 7.231 )]

Dufour FD, Silveira PA, Baxter AG. (2008) Interactions between B Cells and Type 1 NKT Cells in Autoimmune Diabetes. J Immunotoxicology 5: 249-57. [5 (IF = 1.218)]

Fletcher JM#, Jordan MA#, Snelgrove SL, Slattery RM, Dufour FD, Kyparissoudis K, Besra GS, Godfrey DI and Baxter AG (2008) Congenic analysis of the NKT cell control gene Nkt2 implicates the peroxisomal protein Pxmp4. J Immunol 181:3400-12. (# = authors contributed equally) [6 (IF = 5.646)]

Jordan MA, Poulton LD, Fletcher JM  and  Baxter AG. (2009) Allelic variation of Ets1 does not contribute to NK and NKT cell deficiencies in type 1 diabetes susceptible NOD mice. Rev Diabetic Stud 6: 104-116. [journal not indexed]

Fletcher MT, Baxter AG. (2009) Clinical Application of NKT Cell Biology in Type 1 (Autoimmune) Diabetes Mellitus. Immunol Cell Biol 87: 315-23. [3 (IF = 4.2)]

Godfrey DI, Stankovic S, Baxter AG. (2009) Developing NKT cells need their calcium. Nature Immunology 10: 231-233. [2 (IF = 26)]

Godfrey DI, Stankovic S, Baxter AG. (2010) Raising the NKT family. Nature Immunology 11: 197-206. [48 (IF = 26)]

Baune BT, Dannlowski U, Janssen DAG, Jordan MA, Ohrmann P, Bauer J, Domschke K, Arolt V, Kugel H, Baxter AG, Suslow T. (2010) The interleukin 1 beta (IL1B) gene is associated with failure to achieve remission and impaired emotion processing in major depression. Biol Psychiatry. 67(6):543-9. [7 (IF = 8.926)]

Jordan MA, Fletcher JM, Jose R, Chowdhury S, Gerlach N, Allison J and Baxter AG. (2011) Role of SLAM in NKT cell development revealed by transgenic complementation in NOD mice. J Immunol. 2011 Apr 1;186(7):3953-65. [0 (IF = 5.646)]

Berzins SP, Smyth MJ, Baxter AG. (2011) Presumed guilty: NKT cell defects and human disease. Nature Reviews Immunology 11: 131- 142. [7 (IF = 32.245)]

Miranda-Hernandez S, Gerlach N, Fletcher JM, Biros E, Mack M, Körner H  and Baxter AG. (2011) Role for MyD88, TLR2 and TLR9, but not TLR1, TLR4 or TLR6 in Experimental Autoimmune Encephalomyelitis in a Controlled Environment. J Immunol 187: 791-804. [0 (IF = 5.646)]


 
LINKS:

 

Keywords: Immunology, immune, immunogenetics, disease, risk, vaccine, Medical Genomics rResearch Group, Autoimmunity Research Group, James Cook University and the Centenary Institute of Cancer Medicine and Cell Biology, Key words: Genetics, Genomics, Phenomics, Proteinomics, Gene, Autoimmune diabetes, Type 1 diabetes mellitus, childhood diabetes, lupus, systemic lupus erythematosus, haemolytic anaemia, hemolytic anemia, Coombs' test, antinuclear antibodies, renal failure, glomerulonephritis, gastritis, type A gastritis, pernicious anemia, immunology, popular science, biology.