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The aim of this work is to investigate fracture mechanical characteristic of aluminum alloy 6061 by the small punch test in low range of deformation rate. The results of the force-displacement of the puncher curve and scanning electron microscope observation of fracture surface of deformed specimen are used to discuss fracture toughness of the material. The obtained results show that the influence of the displacement rate on the force - displacement of the puncher cannot be clearly seen. The mechanism of fracture properties of aluminum alloy 6061 is quite complicated and there is a large difference between the fracture surface of the top side which contacts with the punch head and the fracture surface of the bottom side. The bottom side shows not only crack in the direction perpendicular to the applied external force but also crack along the direction of the crack ring. The local ductile fracture might dominate to induce the initial crack due to shear stress. Then, the crack spreads via the direction perpendicular to the applied external force as well as along the direction of the crack ring without any dimples. Meanwhile, tensile stress plays an important role in breaking the specimen in half. [ABSTRACT FROM AUTHOR]

The involvement of ©δ TCR-bearing lymphocytes in immunological memory has gained increasing interest due to their functional duality between adaptive and innate immunity. ©δ T effector memory (TEM) and central memory (TCM) subsets have been identified, but their respective roles in memory responses are poorly understood. In the present study, we used subsequent mouse cytomegalovirus (MCMV) infections of αβ T cell deficient mice in order to analyze the memory potential of ©δ T cells. As for CMV-specific αβ T cells, MCMV induced the accumulation of cytolytic, KLRG1+CX3CR1+ ©δ TEM that principally localized in infected organ vasculature. Typifying T cell memory, ©δ T cell expansion in organs and blood was higher after secondary viral challenge than after primary infection. Viral control upon MCMV reinfection was prevented when masking ©δ T-cell receptor, and was associated with a preferential amplification of private and unfocused TCR δ chain repertoire composed of a combination of clonotypes expanded post-primary infection and, more unexpectedly, of novel expanded clonotypes. Finally, long-term-primed ©δ TCM cells, but not ©δ TEM cells, protected T cell-deficient hosts against MCMV-induced death upon adoptive transfer, probably through their ability to survive and to generate TEM in the recipient host. This better survival potential of TCM cells was confirmed by a detailed scRNASeq analysis of the two ©δ T cell memory subsets which also revealed their similarity to classically adaptive αβ CD8 T cells. Overall, our study uncovered memory properties of long-lived TCM ©δ T cells that confer protection in a chronic infection, highlighting the interest of this T cell subset in vaccination approaches. Author summary: Cytomegalovirus (CMV) is a widespread, latent virus that can cause severe organ disease in immune-compromised patients. Anti-CMV memory immune responses are essential to control viral reactivation and/or reinfection events that commonly take place in solid organ transplantation. The role of ©δ T-cell receptor bearing lymphocytes could be crucial in this context where immunosuppressive/ablative treatments cause suboptimal and/or delayed αβ T cell responses. Here we asked whether ©δ T cells could compensate for the absence of αβ T cells in the long-term control of mouse CMV infection. Three months post-primary viral challenge in αβ-T cell deficient mice, ©δ T cells displayed similar features as cytolytic, CMV-specific αβ CD8 T cells. We showed that previous priming with CMV endowed ©δ T cells with an enhanced antiviral potential and that long-term maintenance of ©δ T cell-mediated antiviral protection was dependent on ©δ central memory T cells (TCM). As observed in human, the ©δ T cell response to a secondary CMV challenge generated a private TCR δ repertoire. Finally, our gene expression/accessibility single cell analysis revealed that ©δ TCM shared similar features as their αβ T cell counterpart. Our results sustain the adaptive-like properties of these unconventional T cells and reveal the interest of targeting ©δ TCM subset in novel antiviral vaccination approaches. [ABSTRACT FROM AUTHOR]

Background: The etiology of inflammatory bowel disease (IBD) is unclear but involves both genetics and environmental factors, including the gut microbiota. Indeed, exacerbated activation of the gastrointestinal immune system toward the gut microbiota occurs in genetically susceptible hosts and under the influence of the environment. For instance, a majority of IBD susceptibility loci lie within genes involved in immune responses, such as caspase recruitment domain member 9 (Card9). However, the relative impacts of genotype versus microbiota on colitis susceptibility in the context of CARD9 deficiency remain unknown. Results: Card9 gene directly contributes to recovery from dextran sodium sulfate (DSS)-induced colitis by inducing the colonic expression of the cytokine IL-22 and the antimicrobial peptides Reg3β and Reg3γ independently of the microbiota. On the other hand, Card9 is required for regulating the microbiota capacity to produce AhR ligands, which leads to the production of IL-22 in the colon, promoting recovery after colitis. In addition, cross-fostering experiments showed that 5 weeks after weaning, the microbiota transmitted from the nursing mother before weaning had a stronger impact on the tryptophan metabolism of the pups than the pups' own genotype. Conclusions: These results show the role of CARD9 and its effector IL-22 in mediating recovery from DSS-induced colitis in both microbiota-independent and microbiota-dependent manners. Card9 genotype modulates the microbiota metabolic capacity to produce AhR ligands, but this effect can be overridden by the implantation of a WT or "healthy" microbiota before weaning. It highlights the importance of the weaning reaction occurring between the immune system and microbiota for host metabolism and immune functions throughout life. A better understanding of the impact of genetics on microbiota metabolism is key to developing efficient therapeutic strategies for patients suffering from complex inflammatory disorders. -8ZHpF322gum1G2x3b5Gvy Video Abstract [ABSTRACT FROM AUTHOR]