Net-zero aviation: Transition barriers and radical climate policy design implications

While air transport decarbonization is theoretically feasible, less attention has been paid to the complexity incurred in various ‘transition barriers’ that act as roadblocks to net-zero goals. A total of 40 barriers related to mitigation, management, technology and fuel transition, finance, and governance are identified. As these make decarbonization uncertain, the paper analyzes air transport system's growth, revenue, and profitability. Over the period 1978–2022, global aviation has generated marginal profits of US$20200.94 per passenger, or US$202082 billion in total. Low profitability makes it unlikely that the sector can finance the fuel transition cost, at US$0.5–2.1 trillion (Dray et al. 2022). Four radical policy scenarios for air transport futures are developed. All are characterized by “limitations”, such as CO2 taxes, a carbon budget, alternative fuel obligations, or available capacity. Scenario runs suggest that all policy scenarios will more reliably lead to net-zero than the continued volume growth model pursued by airlines

Dual checkpoint blockade of CD47 and LILRB1 enhances CD20 antibody-dependent phagocytosis of lymphoma cells by macrophages

Antibody-dependent cellular phagocytosis (ADCP) by macrophages, an important effector function of tumor targeting antibodies, is hampered by ‘Don´t Eat Me!’ signals such as CD47 expressed by cancer cells. Yet, human leukocyte antigen (HLA) class I expression may also impair ADCP by engaging leukocyte immunoglobulin-like receptor subfamily B (LILRB) member 1 (LILRB1) or LILRB2. Analysis of different lymphoma cell lines revealed that the ratio of CD20 to HLA class I cell surface molecules determined the sensitivity to ADCP by the combination of rituximab and an Fc-silent variant of the CD47 antibody magrolimab (CD47-IgGσ). To boost ADCP, Fc-silent antibodies against LILRB1 and LILRB2 were generated (LILRB1-IgGσ and LILRB2-IgGσ, respectively). While LILRB2-IgGσ was not effective, LILRB1-IgGσ significantly enhanced ADCP of lymphoma cell lines when combined with both rituximab and CD47-IgGσ. LILRB1-IgGσ promoted serial engulfment of lymphoma cells and potentiated ADCP by non-polarized M0 as well as polarized M1 and M2 macrophages, but required CD47 co-blockade and the presence of the CD20 antibody. Importantly, complementing rituximab and CD47-IgGσ, LILRB1-IgGσ increased ADCP of chronic lymphocytic leukemia (CLL) or lymphoma cells isolated from patients. Thus, dual checkpoint blockade of CD47 and LILRB1 may be promising to improve antibody therapy of CLL and lymphomas through enhancing ADCP by macrophages