In 2001, seventeen professionals set up the manifesto for agile software development. They wanted to define values and basic principles for better software development. On top of being brought into focus, the manifesto has been widely adopted by developers, in software-developing organizations and outside the world of IT. Agile principles and their implementation in practice have paved the way for radical new and innovative ways of software and product development. In parallel, the understanding of the manifesto's underlying principles evolved over time. This, in turn, may affect current and future applications of agile principles. This article presents results from a survey and an interview study in collaboration with the original contributors of the manifesto for agile software development. Furthermore, it comprises the results from a workshop with one of the original authors. This publication focuses on the origins of the manifesto, the contributors' views from today's perspective, and their outlook on future directions. We evaluated 11 responses from the survey and 14 interviews to understand the viewpoint of the contributors. They emphasize that agile methods need to be carefully selected and agile should not be seen as a silver bullet. They underline the importance of considering the variety of different practices and methods that had an influence on the manifesto. Furthermore, they mention that people should question their current understanding of "agile" and recommend reconsidering the core ideas of the manifesto.

Worldwide, an estimated 12 million people are infected with Leishmania spp. and an additional 350 million are at risk of infection. Leishmania are intracellular parasites that cause disease by suppressing macrophage microbicidal responses. Infection can remain asymptomatic or lead to a spectrum of diseases including cutaneous, mucocutaneous, and visceral leishmaniasis. Ultimately, the combination of both pathogen and host factors determines the outcome of infection. Leishmaniasis, as well as numerous other infectious diseases, exhibits sex-related differences that cannot be explained solely in terms of environmental exposure or healthcare access. Furthermore, transcriptomic evidence is revealing that biological sex is a variable impacting physiology, immune response, drug metabolism, and consequently, the progression of disease. Herein, we review the distribution, morbidity, and mortality among male and female leishmaniasis patients. Additionally, we discuss experimental findings and new avenues of research concerning sex-specific responses in cutaneous and visceral leishmaniasis. The limitations of current therapies and the emergence of drug-resistant parasites underscore the need for new treatments that could harness the host immune response. As such, understanding the mechanisms driving the differential immune response and disease outcome of males versus females is a necessary step in the development of safer and more effective treatments against leishmaniasis.

causes visceral leishmaniasis (VL) in Brazil. We previously observed that VL is more common in males than females living in endemic neighborhoods, despite similar exposure. Using a larger sample, we document that VL is more common in males than females, but only after puberty. BALB/c and C57BL/6 mouse models confirmed that there is a biological basis for male susceptibility to symptomatic VL, showing higher parasite burdens in males than females. Female C57BL/6 mice generated more antigen-induced cytokines associated with curative responses (interferon-γ, interleukin [IL]-1β). Males expressed higher levels of IL-10 and tumor necrosis factor, which are linked to exacerbated disease. Different parasite lines entered or survived at a higher rate in macrophages of male- than female-origin. These results suggest that males are inherently more susceptible to than females and that mice are a valid model to study this sex-dependent difference.

SUMMARY Lipid bodies (LBs) are intracellular accumulations of neutral lipids surrounded by a single membrane. These organelles are involved in the production of eicosanoids, which modulate immunity by either promoting or dampening inflammatory responses. Leishmania infantum, the etiological agent of visceral leishmaniasis in Brazil, is an intracellular parasite that causes disease by suppressing macrophage microbicidal responses. C57BL/6 mouse bone marrow-derived macrophages infected with L. infantum strain LcJ had higher numbers of LB+ cells (P<0.0001) and total LBs than non-infected cultures. Large (> 3μm) LBs were present inside parasitophorous vacuoles (PVs). These results contrast with those of L. infantum-infected BALB/c macrophages, in which the only LBs are derived from parasite, not macrophage origin. Increased LBs in C57BL/6 macrophages in close association with parasites would position host LBs where they could modulate L. infantum infection. These results imply a potential influence of the host genetics on the role of LBs in host-pathogen interactions. Overall, our data support a model in which the expression, and the role of LBs upon infection, ultimately depends of the specific combination of host-pathogen interactions.