A recent review of pancreatic carcinoma stated, “In spite of poor results, we must continue to search actively for more accurate methods of diagnosis and better methods of treatment”1; in light of this, further study of immunotherapy may be appropriate.

Gut readers will not be surprised to see this article as, every decade, immunotherapy becomes a “hot” topic and, as such, generates short lived enthusiasm. Thus, BCG, tumour lysates, and even interleukin (IL) 2 as a single agent, have recently been of interest to those involved in scientific research. Immunotherapy is currently at the fore as we can now, actively or passively, stimulate the immune system of patients with pancreatic cancer, creating an immunotherapeutic regimen which may be partially or completely effective in curing the disease. Why such optimism? Recently, developments in genetic engineering techniques have lead to breakthroughs identifying tumour antigens, the description of numerous cytokines (approximately 25, including IL 1–18, tumour necrosis factor (TNF) o/o, interferons (IFN) α, β, γ, and others), and more recently, chemokines, of which there are more than 30, including their receptors.

Using recombinant techniques, it is now possible to produce large amounts of antigens and cytokines for preclinical and clinical studies. Furthermore, these reagents, and the crystallisation of MHC class I and class II molecules, have shown us how antigens enter cells, are degraded into peptides, and presented by class I or class II molecules.2 ,3 This process is particularly important because class I molecules present peptides to CD8 T cells. In tumour immunotherapy, this may give rise to killer T lymphocytes which function either by killing and/or inducing cytokine production, particularly IFN γ, TNF α, IL-2, and IL-12—that is, a Th1 response. The most effective therapy also requires CD4 mediated T cell help, with recognition occurring through longer …