IL-12 is the typical cytokine that can induce Th1 cells from naive cells. See also this paper:

http://www.ncbi.nlm.nih.gov/pubmed/12563297

Interleukin-12 and the regulation of innate resistance and adaptive immunity.

Trinchieri G

Nat Rev Immunol. 2003 Feb; 3(2):133-46.

Please review the following:

The Th17 family: flexibility follows function.  Immunol Rev. 2013 Mar;252(1):89-103.

Basu R1, Hatton RD, Weaver CT.

Abstract

Discovery of the T-helper 17 (Th17) subset heralded a major shift in T-cell biology and immune regulation. In addition to defining a new arm of the adaptive immune response, studies of the Th17 pathway have led to a greater appreciation of the developmental flexibility, or plasticity, that is a feature of T-cell developmental programs. Since the initial finding that differentiation of Th17 cells is promoted by transforming growth factor-β (TGFβ), it became clear that Th17 cell development overlapped that of induced regulatory T (iTreg) cells. Subsequent findings established that Th17 cells are also unusually flexible in their late developmental programming, demonstrating substantial overlap with conventional Th1 cells through mechanisms that are just beginning to be understood but would appear to have important implications for immunoregulation at homeostasis and in immune-mediated diseases. Herein we examine the developmental and functional features of Th17 cells in relation to iTreg cells, Th1 cells, and Th22 cells, as a basis for understanding the contributions of this pathway to host defense, immune homeostasis, and immune-mediated disease.

Regulation of antitumor immune responses by the IL-12 family cytokines, IL-12, IL-23, and IL-27. Clin Dev Immunol. 2010;2010. pii: 832454.

Xu M1, Mizoguchi I, Morishima N, Chiba Y, Mizuguchi J, Yoshimoto T.

Abstract

The interleukin (IL)-12 family, which is composed of heterodimeric cytokines including IL-12, IL-23, and IL-27, is produced by antigen-presenting cells such as macrophages and dendritic cells and plays critical roles in the regulation of helper T (Th) cell differentiation. IL-12 induces IFN-γ production by NK and T cells and differentiation to Th1 cells. IL-23 induces IL-17 production by memory T cells and expands and maintains inflammatory Th17 cells. IL-27 induces the early Th1 differentiation and generation of IL-10-producing regulatory T cells. In addition, these cytokines induce distinct immune responses to tumors. IL-12 activates signal transducers and activator of transcription (STAT)4 and enhances antitumor cellular immunity through interferon (IFN)-γ production. IL-27 activates STAT1, as does IFN-γ and STAT3 as well, and enhances antitumor immunity by augmenting cellular and humoral immunities. In contrast, although exogenously overexpressed IL-23 enhances antitumor immunity via memory T cells, endogenous IL-23 promotes protumor immunity through STAT3 activation by inducing inflammatory responses including IL-17 production.

The IL-12/IL-23 axis and its role in Th17 cell development, pathology and plasticity in arthritis. Curr Opin Investig Drugs. 2009 May;10(5):452-62.

Cornelissen F1, van Hamburg JP, Lubberts E.

Abstract

Rheumatoid arthritis (RA) was originally thought to be a T-helper (Th)1-, not a Th2-, associated disorder; however, it currently is unclear whether RA is a Th1- and/or Th17-mediated disease, and what the contributions of these T-cell subsets are in the pathogenesis of RA. Results from studies using different arthritis models have demonstrated that IL-17-producing T-cells are the dominant cell type in the development of arthritis. In addition, a critical role of the IL-23/IL-17 axis in the progression to chronic destructive arthritis has been demonstrated. Interestingly, Th1 and Th17 cells both may have unique pathogenic potential, and the recent insights into T-cell plasticity may change the understanding of the role of T-cell subsets in chronic autoimmune diseases.

From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited. Immunol Rev. 2008 Dec;226:132-46.

Boniface K1, Blom B, Liu YJ, de Waal Malefyt R.

Abstract

Protracted inflammation leading to dysregulation of effector T-cell responses represents a common feature of a wide range of autoimmune diseases. The interleukin-12 (IL-12)/T-helper 1 (Th1) pathway was thought to be responsible for the pathogenesis of multiple chronic inflammatory diseases, including psoriasis, inflammatory bowel disease, arthritis, or multiple sclerosis, mainly through their production of interferon-gamma and its effects on macrophage activation and chemokine production. However, this initial concept of T-cell-mediated chronic inflammation required an adjustment with the discovery of an IL-12-related cytokine, designated IL-23. IL-23 was rapidly recognized for its involvement in the establishment of chronic inflammation and in the development of a Th cell subset producing IL-17, designated Th17, which is distinct from the previously reported Th1 and Th2 populations. This review aims to describe the characterization of IL-23 and its receptor, its biological activities, as well as its involvement in the development of human Th17 cells and autoimmunity.

IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu Rev Immunol. 2007;25:821-52.

Weaver CT1, Hatton RD, Mangan PR, Harrington LE.

Abstract

Since its conception two decades ago, the Th1-Th2 paradigm has provided a framework for understanding T cell biology and the interplay of innate and adaptive immunity. Naive T cells differentiate into effector T cells with enhanced functional potential for orchestrating pathogen clearance largely under the guidance of cytokines produced by cells of the innate immune system that have been activated by recognition of those pathogens. This secondary education of post-thymic T cells provides a mechanism for appropriately matching adaptive immunity to frontline cues of the innate immune system. Owing in part to the rapid identification of novel cytokines of the IL-17 and IL-12 families using database searches, the factors that specify differentiation of a new effector T cell lineage-Th17-have now been identified, providing a new arm of adaptive immunity and presenting a unifying model that can explain many heretofore confusing aspects of immune regulation, immune pathogenesis, and host defense.

Dear Ming, 

IFNg is very weak compared to IL12 for inducing IFNg, probably because of a synergy between IL12 signaling and IFNg signaling on Tbet or IFNg promoters, so only one is not enough. Hopefully IL12 can initiate a weak IFNg production that autoamplify itself whereas IFNg is not able to induce IL12 production by T cells

IL12 works in vitro but it doesn't mean that this is the only signal that T cells receive to become Th1 in vivo ... so probably there are other ways to create Th1s without IL12, and then comes the question if all the Th1s in vivo are the same ... For instance, certain viral infections manage to initiate a Th1 response in IL12 deficient mice,  

If I would try alternative Th1 inducing cytokines, I would try a combination of IFNa/b, IFNg, IL18 or IL27, 

Best,

Dear Ming,

You will also accept that especially in relevance, human body is very dynamic. Not only IL-12 apart from interferons are only responsible for stimulation of naive T cells to Th1; Much more research is awaited for understanding more transducers of the Pathway.