Mitogen activation of human peripheral T lymphocytes induces the formation of new cyclic AMP response element-binding protein nuclear complexes.

Patrik, Wollberg; Söderqvist, Henrik; Nelson, Bruce R.

doi:10.1016/s0021-9258(17)32080-x

Cited by 19 publications

(1 citation statement)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is worth noting that the opposing forces of the sympathetic and parasympathetic nervous systems are not mere discord but rather a delicate interplay, a harmonic tension that underpins the exquisite balance of the immune response. The sympathetic nerve employs cyclic AMP (cAMP) as its intracellular second messenger, while the parasympathetic nerve utilizes cyclic GMP (cGMP) [41][42][43]. Though both are derived from purines, the direction of their NH2 groups is opposite, akin to the complementary tones of a major and minor chord.…”

Section: The Autonomic Nervous System: Striking the Chord Of Inflamma...mentioning

confidence: 99%

Understanding the Immune System’s Intricate Balance: Activation, Tolerance, and Self-Protection

2024

Preprint

View full text Add to dashboard Cite

The mechanism of immune activation and de-activation is very important. Host should trigger effective immunity against pathogen infection. And, host cannot trigger immunity against self-antigens that will lead to detrimental autoimmune disorders. Spleen and liver have opposite roles in mediating immune responses. Spleen is the organ involving in immune activation, and liver is the organ involving in immune de-activation. Sympathetic nerve system and parasympathetic nerve system have opposite roles in mediating immune responses. Sympathetic nerve system is involving in pro-inflammatory, and parasympathetic nerve system is involving in anti-inflammatory. ACTH and glucocorticosteroid have opposite roles in mediating immune responses. ACTH is involving in activating adaptive immunity with inhibiting innate immunity, and glucocorticosteroid is involving in activating innate immunity with inhibiting adaptive immunity. The molecular chaperons, heat shock proteins, which are induced by fever, have the vital roles in immune activation. On the contrary, IgD B cells and gamma-delta T cells are causing immune de-activation via the mechanism of clonal anergy. These mechanism can help us the know the work of immunological pathways better for better control of infectious diseases and autoimmune disorders.

show abstract

Section: The Autonomic Nervous System: Striking the Chord Of Inflamma...mentioning

confidence: 99%

Understanding the Immune System’s Intricate Balance: Activation, Tolerance, and Self-Protection

2024

Preprint

View full text Add to dashboard Cite

show abstract

Involvement of cAMP in CD3 T cell receptor complex‐ and CD2‐mediated apoptosis of human thymocytes

et al. 1995

View full text Add to dashboard Cite

During intrathymic T cell development, elimination of autoreactive T cell clones by programmed cell death (PCD or apoptosis) is an essential mechanism for self tolerance. The precise intracellular second messengers that lead to this process remain to be determined. In the present work, we show that treatment of freshly isolated thymocytes with an antagonist of the cAMP pathway, the Rp-cAMP, significantly decreases spontaneous death by apoptosis of human thymocytes in vitro. Addition of Rp-cAMP also rescues thymocytes from activation-induced apoptosis following the ligation of surface CD3/T cell receptor complex or CD2 antigens. A cAMP analog, the dibutyryl(Dibut)-cAMP increases PCD of human thymocytes in a dose-dependent manner. Growth and rescue from PCD of thymocytes in the presence of interleukin (IL)-2 or IL-4 are also enhanced by Rp-cAMP and inhibited by Dibut-cAMP. Finally, we detect substantial levels of intracellular cAMP in freshly isolated thymocytes. This study reveals the involvement of cAMP as a second messenger during the apoptosis of normal human thymocytes.

show abstract

CREB function is required for normal thymic cellularity and post‐irradiation recovery

et al. 2004

View full text Add to dashboard Cite

Recent generation of genetically modified Creb1 mutant mice has revealed an important role for CREB (cAMP responsive element binding protein) and the related proteins CREM (cAMP responsive element modulator) and ATF1 (activating transcription factor 1) in cell survival, in agreement with previous studies using overexpression of dominant-negative CREB (dnCREB). CREB and ATF1 are abundantly expressed in T cells and are rapidly activated by phosphorylation when T cells are stimulated through the T cell antigen receptor. We show that T cell-specific loss of CREB in mice, in combination with the loss of ATF1, results in reduced thymic cellularity and delayed thymic recovery following sublethal irradiation but no changes in T cell development or activation. These data show that loss of CREB function has specific effects on thymic T lymphocyte proliferation and homeostasis in vivo.

show abstract

Mitogen activation of human peripheral T lymphocytes induces the formation of new cyclic AMP response element-binding protein nuclear complexes.

Cited by 19 publications

References 48 publications

Understanding the Immune System’s Intricate Balance: Activation, Tolerance, and Self-Protection

Understanding the Immune System’s Intricate Balance: Activation, Tolerance, and Self-Protection

Involvement of cAMP in CD3 T cell receptor complex‐ and CD2‐mediated apoptosis of human thymocytes

CREB function is required for normal thymic cellularity and post‐irradiation recovery

Contact Info

Product

Resources

About