M Arifur Rahman

Senior research professional with proven track record in conducting and overseeing cutting-edge projects. Skilled in data analysis, research methodologies, and project management, consistently delivering high-impact results. Strong focus on team collaboration, adaptability, and achieving objectives efficiently. Known for reliability and ability to meet evolving needs while maintaining high standards and precision.

• Supervised team of 5 research staff members.
• Collaborated with industrial partners in the development of an effective immunotherapy for Lupus and Sjogren's Syndrome.

• 2023- Member, The Australian and New Zealand Society for Immunology (ASI)
• 2020- Member, ‘Class of 2020’- The University of Queensland Future Leaders program
• 2017- Member, Australian Society for Medical Research (ASMR)
• 2011- Member, American Society for Microbiology (ASM)

• Co-supervisor, BSc Honours project: The role of TACI and high fibre diet in systemic lupus erythematosus (SLE), The University of Queensland, 2023-2024 (Graduated with Thesis Distinction).
• Co-supervisor, BSc Honours project: The role of specialised metabolite-releasing diet in systemic lupus erythematosus (SLE), The University of Queensland, 2024 (Current).
• Co-supervisor, BSc Honours project: The role of TACI in T cell development and function, The University of Queensland, 2024 (Current).

• Publication record:
• Number of publications: 16
• Citations: 419, h-index: 10, i-10 index: 10 (Google Scholar)
• Https://scholar.google.com.au/citations?hl=en&user=kNLELp4AAAAJ&scilu=&scisig=ANI4uE0AAAAAZtaCjIDpaGviOoKTaOTv6tjqYlE&gmla=AC6IMd-UzIT9goP3kFBs-L8AnqAnKQSa67CEfu0o_kjFotMrSoUVnnUdp0JFpTsYQQ7gkckmMk8GmlMsEUvvqXQSzM5mNT2aOj7Asc&scisund=4244652861785463575

• I. Mucosal-Associated Invariant T (MAIT) cells are highly activated in duodenal tissue of humans with Vibrio cholerae O1 infection: A preliminary report.
• II. Plasma and memory B cell responses targeting O-specific polysaccharide (OSP) are associated with protection against Vibrio cholerae O1 infection among household contacts of cholera patients in Bangladesh.
• III. O-specific polysaccharide (OSP)-specific memory B cell responses in young children, older children and adults infected with Vibrio cholerae O1 Ogawa in Bangladesh.
• IV. Plasma Leptin Levels in Children Hospitalized with Cholera in Bangladesh.
• V. Circulating Mucosal Associated Invariant T cells are Activated in Vibrio cholerae O1 Infection and Associated with Lipopolysaccharide Antibody Responses.
• VI. Antigen-Specific Memory B-cell Responses to Enterotoxigenic Escherichia coli Infection in Bangladeshi Adults.
• VII. Immune responses to the O-specific polysaccharide and lipopolysaccharide of Vibrio cholerae O1 in cholera vaccinees and comparison to responses in patients with cholera in Bangladesh.
• I. Genetically encoded Runx3 and CD4+ intestinal epithelial lymphocyte deficiencies link SKG mouse and human predisposition to spondyloarthropathy.
• II. Mediation of Interleukin-23 and Tumor Necrosis Factor-Driven Reactive Arthritis by Chlamydia-Infected Macrophages in SKG Mice.
• III. Inflammasome activation in Ankylosing Spondylitis is associated to gut dysbiosis.
• IV. The SKG model of Spondyloarthritis.
• V. Pro-inflammatory CX3CR1+ CD59+ TL1A+ IL-23+ monocytes are expanded in patients with Ankylosing Spondylitis and modulate ILC3 immune functions.
• VI. A fat and sugar-enriched diet rapidly and persistently alters the fecal microbial community, intestinal mucosal integrity and intestinal immunity.
• VII. IL-27 driven Type 1 regulatory T cells control autoreactive T helper-17 cell expansion in SKG mice.
• I. A convergent evolutionary pathway attenuating cellulose production drives enhanced virulence in some bacteria.
• II. An unappreciated cell survival-independent role for BAFF initiating Chronic Lymphocytic Leukemia.
• III. Interleukin-22 suppresses major histocompatibility complex II in mucosal epithelial cells.
• IV. IL-20 Activates ERK1/2 and suppresses splicing of X-box Protein-1 in Intestinal Epithelial Cells but does not Improve Pathology in Acute or Chronic Models of Colitis.