The quantum model of T‐cell activation: Revisiting immune response theories

Abstract

Our understanding of the immune response is far from complete, missing out on more detailed explanations that could be provided by molecular insights. To bridge this gap, we introduce the quantum model of T‐cell activation. This model suggests that the transfer of energy during protein phosphorylation within T cells is not a continuous flow but occurs in discrete bursts, or ‘quanta’, of phosphates. This quantized energy transfer is mediated by oscillating cycles of receptor phosphorylation and dephosphorylation, initiated by dynamic ‘catch‐slip’ pulses in the peptide‐major histocompatibility complex‐T‐cell receptor (pMHC‐TcR) interactions. T‐cell activation is predicated upon achieving a critical threshold of catch‐slip pulses at the pMHC‐TcR interface. Costimulation is relegated to a secondary role, becoming crucial only when the frequency of pMHC‐TcR catch‐slip pulses does not meet the necessary threshold for this quanta‐based energy transfer. Therefore, our model posits that it is the quantum nature of energy transfer—not the traditional signal I or signal II—that plays the decisive role in T‐cell activation. This paradigm shift highlights the importance of understanding T‐cell activation through a quantum lens, offering a potentially transformative perspective on immune response regulation.

Effective anti-tumor immune responses are orchestrated by immune cell partnership network that functions through tissue homeostatic pathways, not direct cytotoxicity

“…Only 5% of T cells, NKT cells and NK cells produced TRAIL or Fas-L, not for targeting the tumor but for targeting the hepatic structural cells turn over as hepatic homeostasis. Such tissue-based activation of the immune response is evident from the presence of tissue-resident T memory cells (Trm) 54 which can be explained by the quantum model of T cell activation recently proposed by the last author 55 . Also, the primary function of immune responses has been proposed to be participating in homeostasis of their target cells [56][57][58][59][60][61] .…”