Jan Andersson

Hodgkin's lymphoma (HL) is a lymphoproliferative disorder of B-lymphocytes. Epstein-Barr virus (EBV) antigens can be detected in tumours in up to 40% of all HL cases. Patients with EBV-associated HL also show increased levels of EBV-infected B-lymphocytes in blood compared with normal individuals and non-EBV-associated HL cases. A peculiar pattern of restricted EBV-antigen expression, dominated by latent membrane protein-1 (LMP-1), LMP-2 and EBV nuclear antigen-1, is the characteristic feature of tumour-specific Hodgkin/Reed-Sternberg cells. This knowledge has generated studies examining adoptive immunotherapy of autologous or allogeneic cytotoxic T-cells for the treatment of refractory EBV-positive HL cases. Whether aborted EBV or another infectious aetiology is involved in non-EBV-associated HL cases remains an open question.

Acute HIV-1 infection results in profound depletion of CD4+ memory T cells in lymphoid tissue (LT) and subsequent persistent replication in activated CD4+ T cells despite induction of an HIV-specific cell-mediated immune response. Interferon-α, proinflammatory cytokines, and β-chemokine production is present in LT. However, impaired expression of co-stimulatory molecules including CD80, CD86, and CD40L may contribute to low polyfunctional CD4+ T cell as well CD8+ T-cell activity. Accumulation of regulatory CD4+ T cells in LT may add to the lack of HIV-specific CD4+ T-cell proliferation and dysfunctional cytotoxic CD8+ T-cell response in LT.

: Sepsis is the third leading cause of death in the developed world. Despite recent advances in intensive care treatment and the discovery of antibiotics, sepsis remains associated with a high mortality rate. The pathogenesis of sepsis is characterized by an overwhelming systemic inflammatory response that is central to the development of lethal multiple organ failure. This volume of the Journal of Internal Medicine contains three reviews addressing novel aspects of a system we are only beginning to understand – the interactions between the immune and the nervous systems, the ‘neuro‐immune axis’. Tracey (Nature 2002; 420: 853) recently discovered that the nervous system, through the vagus nerve, can modulate circulating TNF‐α levels induced by microbial invasion or tissue injury. This cholinergic anti‐inflammatory pathway is mediated primarily by nicotinic acetylcholine receptors on tissue macrophages – the pathway leads to decreased production of proinflammatory cytokines. The author reports that treatment with the acetylcholine receptor agonist, nicotine, modulates this system and reduces mortality in ‘established’ sepsis. Watkins and Maier (J Intern Med 2005; 257: 139) illustrate that pathological pain (induced by inflammation) is not simply a strict neuronal phenomenon, but is a component of the immune response, and is modulated by peripheral immune cells and spinal cord glia cells. This may be of importance for future development of novel drugs for neuropathic pain as well as our understanding of increased risks for infections in anaesthetic skin areas. Blalock (J Immunol 1984; 132: 1067) elucidates the possibility that the immune system actually functions as the sixth sense, sensing microbes and microbial toxins that we cannot see, hear, taste, touch or smell. Activation of the sympathetic nervous system also has predominantly anti‐inflammatory effects that are mediated through direct nerve to immune cell interaction or through the adrenal neuro‐endocrine axis.