Seminar series speakers 2023 - 2024

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

​The mucosae represent the border between our body and the environment, and they act as the first barrier against infections. Therefore, inflammatory responses must be tightly regulated to combat infection without causing excessive self-damage or interfering with the repair process. An imbalance in these processes could result in the loss of barrier function and tissue functionality. Achille Broggi and his team study the interplay between the immune system and the mucosal layer, with a particular interest in understanding how immune mediators production and functions are regulated in the intestinal mucosa and how they regulate the pathogenesis of inflammatory bowel disease (IBD).

The immune system mounts destructive responses to protect the host from threats, including pathogens and tumours. However, a trade-off emerges: if immune responses cause too much damage, they can compromise host tissue function. Conversely, if they fail to generate sufficient damage, the host may succumb to a given threat. The Wong lab investigates how coordinated communication between cells gives rise to dynamic circuits that steer ongoing immune responses toward desired target values, both in time and space. To this end, we employ various interdisciplinary methods—including advanced fluorescence microscopy, computational modelling, and inducible gene perturbations—to resolve, model, and manipulate immune cell behaviours directly in situ. Ultimately, we aim to understand how imbalanced circuit functions lead to immune-related disorders, including autoimmunity, chronic infection, and cancer.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Ana Luisa Correia is an enthusiastic Cancer Biologist with a main interest in understanding what makes a tissue favorable or not to metastasis, and leverage this biology into therapeutic interventions that reliably prevent the emergence of metastases in patients with cancer. Anahas developed a tool to follow dormant disseminated tumor cells live, offering opportunities to investigate the anatomical distribution, composition and dynamics of dormant reservoirs within and across distant sites. This approach has steered the discovery of a pivotal role for a part of the innate branch of the immune system, the natural killer cells, in luling disseminated tumor cells into dormancy, and how disruption in liver physiology breaches the NK cell barrier to metastasis. This provides a foundational framework for studying the dynamics of antimetastatic innate immunity within and across sites, which the Correia Lab has been pursuing at the Champalimaud Foundation in Lisbon.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

Dr. Covarrubias is a macrophage biologist with expertise in immuno-metabolism, and how inflammation and metabolism are integrated to regulate metabolic health and disease states including aging. Dr. Covarrubias identified the nutrient-sensing Akt-mTORC1 pathway as a critical regulator of macrophage polarization. He also showed that activation of the Akt-mTORC1 target ACLY catalyzes the increase in macrophage cytosolic/nuclear pools of acetyl-CoA. These findings suggest how nutrient and metabolic status can fine-tune macrophage function via nutrient sensing pathways. Dr. Covarrubias’ recent work is focused on how diet and aging-related inflammation impacts the aging process. In a recent manuscript he showed that the decline of NAD+ during aging is driven by the activation of tissue resident macrophages via senescent cells. As senescent cells progressively accumulate in aging tissues, these results highlight a new causal link between visceral tissue senescence, NAD+, and immuno-metabolic dysregulation during aging, an active area of investigation in the Covarrubias Lab at UCLA.

The Zhou lab investigates the intricate immune circuits that exist between tumors and the related immune organs. Our primary focus lies in understanding the generation and perturbation of the adaptive anti-tumor response during tumor initiation and progression. At the age of immunotherapy era, we also delve into comprehending the immunological mechanisms underlying immune regimen treatments, such as cytokines and cellular therapies. Furthermore, our lab pursues pharmacological designing novel molecules that align with these immunological insights. Our ultimate goal is to tackle cancer "from bench to bed" and foster new hope in patients.