Potentiation of Vaccines Through Effective Adjuvant Formulations and Manipulation of the Immune Response

Hughes, H. P. A.; Babiuk, Lorne A.

doi:10.1007/978-1-4899-1450-7_6

Cited by 2 publications

(1 citation statement)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other potential adjuvants which induce a type 1 or type 2 cytokine bias (e.g., Brucella abortus induction of IFN-␥) are also under study (5,30,143). Hughes and Babiuk have recently reviewed the immunologic effects of conventional and novel vaccine adjuvants, within the context of cytokine production (175). In addition to adjuvants, vaccine dose (low dose versus high dose) may be critical in the optimization of cellular and humoral immune responses against certain diseases, with low-dose antigen usually considered to elicit more CMI than humoral immunity (38,39,328).…”

Section: Bench To Bedside and Clinic: Implications Of The Type 1-typementioning

confidence: 99%

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases.

Lucey¹,

Clerici²,

Shearer³

1996

Clinical Microbiology Reviews

125

153

View full text Add to dashboard Cite

Section: Bench To Bedside and Clinic: Implications Of The Type 1-typementioning

confidence: 99%

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases.

Lucey¹,

Clerici²,

Shearer³

1996

Clinical Microbiology Reviews

125

153

View full text Add to dashboard Cite

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases

1996

View full text Add to dashboard Cite

In the mid-1980s, Mosmann, Coffman, and their colleagues discovered that murine CD4+ helper T-cell clones could be distinguished by the cytokines they synthesized. The isolation of human Th1 and Th2 clones by Romagnani and coworkers in the early 1990s has led to a large number of reports on the effects of Th1 and Th2 on the human immune system. More recently, cells other than CD4+ T cells, including CD8+ T cells, monocytes, NK cells, B cells, eosinophils, mast cells, basophils, and other cells, have been shown to be capable of producing "Th1" and "Th2" cytokines. In this review, we examine the literature on human diseases, using the nomenclature of type 1 (Th1-like) and type 2 (Th2-like) cytokines, which includes all cell types producing these cytokines rather than only CD4+ T cells. Type 1 cytokines include interleukin-2 (IL-2), gamma interferon, IL-12 and tumor necrosis factor beta, while type 2 cytokines include IL-4, IL-5, IL-6, IL-10, and IL-13. In general, type 1 cytokines favor the development of a strong cellular immune response whereas type 2 cytokines favor a strong humoral immune response. Some of these type 1 and type 2 cytokines are cross-regulatory. For example, gamma interferon and IL-12 decrease the levels of type 2 cytokines whereas IL-4 and IL-10 decrease the levels of type 1 cytokines. We use this cytokine perspective to examine human diseases including infections due to viruses, bacteria, parasites, and fungi, as well as selected neoplastic, atopic, rheumatologic, autoimmune, and idiopathic-inflammatory conditions. Clinically, type 1 cytokine-predominant responses should be suspected in any delayed-type hypersensitivity-like granulomatous reactions and in infections with intracellular pathogens, whereas conditions involving hypergammaglobulinemia, increased immunoglobulin E levels, and/or eosinophilia are suggestive of type 2 cytokine-predominant conditions. If this immunologic concept is relevant to human diseases, the potential exists for novel cytokine-based therapies and novel cytokine-directed preventive vaccines for such diseases.

show abstract

Potentiation of Vaccines Through Effective Adjuvant Formulations and Manipulation of the Immune Response

Cited by 2 publications

References 87 publications

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases.

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases.

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases

Contact Info

Product

Resources

About