**Author details**

*Cells of the Immune System*

**Figure 3.**

*included.*

formation [68].

**8. Conclusions**

*Modulation of T lymphocyte function by TGFβ factor and its importance in Th1-mediated diseases. TGFb released by different types of regulatory cells modulates the inflammatory activity of all effector cells, Th1 cells* 

reported inversely correlated with cardiovascular and psoriatic severity.

deficient mice developed multiple inflammatory diseases [64–66].

The T-regulatory activity (Treg) is pathologically low in both psoriasis and atherosclerosis [60]. The activity of pathogenic T cells is regulated by Treg cells activity via IL-10 and TGFβ [61]. The TGFβ inhibits Th1, and Th2 differentiation favors Th1 and Th17 hyperactivity [62] in both pathologies [60]. The increase in TGFβ [63] was

The critical role of TGFβ and Treg cells was evidenced by the finding that TGFβ-

Both nTreg cells and Tr1-induced cells are able to produce IL10. The relevance of IL10 was evidenced by the specific blocking experiments of lymphocyte IL-10 triggering protection against inflammatory processes. The Tr1 cells expressing IL-10 require the presence of TGFα [67]. Regarding Th2-mediated counterregulation, the Th2 produces anti-inflammatory IL-4, IL-5, and IL-13 which decrease Th1 cells activity. The proinflammatory, metabolic, and systemic mechanisms that operate in the pathogenesis of psoriatic disease may explain the accelerated atherosclerotic process in these patients (**Figure 3**). Serum level of proinflammatory cytokines can increase cell-mediated immunity, which upon decreased regulatory Th2 activity and Treg level promote endothelial infiltration of inflammatory cells and plaque

The heterogeneity of the T cells in general and TCD4 helper, in particular, may

reflect divergent pathways in response to epigenetic factors or different stages of a unique differentiation pathway. Adhesion molecules, e.g., LFA1 and ICAM, CCR and CXCR chemokine receptors, and activation molecules, among others of

The heterogeneity may obey to a programmed developmental process or to microenvironmental stimulation. Immunosuppressive or stimulatory signals like cytokines seem crucially involved though both may participate. This information is expected to shed light on the possible pathogenic role of Th cells in human inflam-

The relationships between the classic Th1/ Th2 and the more recently defined Th17/iTreg/ Tfh/Th9 cells and effector-regulatory cell interactions need clarifica-

tion regarding their pathogenic role in human inflammatory diseases.

undetermined function, reflect the transition.

matory diseases beyond the Th1/Th2 paradigm.

**42**

Rodolfo Alberto Kölliker Frers1,2, Matilde Otero-Losada1 \*, María Inés Herrera1,3, Sabrina Porta2 , Vanesa Cosentino2 , Eduardo Kerzberg2 , Lucas Udovin1 and Francisco Capani1,3

1 Institute of Cardiological Research, University of Buenos Aires, National Research Council, ININCA, UBA-CONICET, Buenos Aires, Argentina

2 Hospital Ramos Mejía, Buenos Aires, Argentina

3 Pontifical Catholic University of Argentina, Buenos Aires, Argentina

\*Address all correspondence to: molly1063@gmail.com

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
