Does zero temperature decide on the nature of the electroweak phase transition?

Taking on a new perspective of the electroweak phase transition, we investigate in detail the role played by the depth of the electroweak minimum (“vacuum energy difference”). We find a strong correlation between the vacuum energy difference and the strength of the phase transition. This correlation only breaks down if a negative eigen-value develops upon thermal corrections in the squared scalar mass matrix in the broken vacuum before the critical temperature. As a result the scalar fields slide across field space toward the symmetric vacuum, often causing a significantly weakened phase transition. Phenomenological constraints are found to strongly disfavour such sliding scalar scenarios. For several popular models, we suggest numerical bounds that guarantee a strong first order electroweak phase transition. The zero temperature phenomenology can then be studied in these parameter regions without the need for any finite temperature calculations. For almost all non-supersymmetric models with phenomenologically viable parameter points, we find a strong phase transition is guaranteed if the vacuum energy difference is greater than −8.8 × 107 GeV4. For the GNMSSM, we guarantee a strong phase transition for phenomenologically viable parameter points if the vacuum energy difference is greater than −6.9×107 GeV4. Alternatively, we capture more of the parameter space exhibiting a strong phase transition if we impose a simultaneous bound on the vacuum energy difference and the singlet mass

Antigen presentation safeguards the integrity of the hematopoietic stem cell pool

Hematopoietic stem and progenitor cells (HSPCs) are responsible for the production of blood and immune cells. Throughout life, HSPCs acquire oncogenic aberrations that can cause hematological cancers. Although molecular programs maintaining stem cell integrity have been identified, safety mechanisms eliminating malignant HSPCs from the stem cell pool remain poorly characterized. Here, we show that HSPCs constitutively present antigens via major histocompatibility complex class II. The presentation of immunogenic antigens, as occurring during malignant transformation, triggers bidirectional interactions between HSPCs and antigen-specific CD4(+4) T cells, causing stem cell proliferation, differentiation, and specific exhaustion of aberrant HSPCs. This immunosurveillance mechanism effectively eliminates transformed HSPCs from the hematopoietic system, thereby preventing leukemia onset. Together, our data reveal a bidirectional interaction between HSPCs and CD4(+4) T cells, demonstrating that HSPCs are not only passive receivers of immunological signals but also actively engage in adaptive immune responses to safeguard the integrity of the stem cell pool