2 Identical lanes of analyzed scRNAseq. Raw fastq's are not available. Lane 1 Visualized but due to overlapping headers Lane 2 data is included in the additional files section. H5 files are also available in the additional files section. Both sets of files needed a (.txt) extension to trick SCP. They are working on a solution to allow MTX and H5 files as additional files. Both Lanes were used in the final analysis to create the rds object, which is linked and downloadable.

Each identical lane had 4 samples. This is the overview of the makeup of those samples

1. Whole blood from human patient, 24c5 FC Variant SEHFST LS, H37Rv MTB Strain
2. Whole blood from human patient, 24c5 FC Variant IgG1, H37Rv MTB Strain
3. Whole blood from human patient, no antibody, H37Rv MTB Strain
4. Whole blood from human patient, no antibody, no TB

Link to metadata for all of this publications data files: https://fairdomhub.org/studies/1089 

Abstract: Novel vaccination and therapeutic strategies are urgently needed to mitigate the tuberculosis (TB) epidemic. While extensive efforts have focused on potentiating cell-mediated immunity to control Mycobacterium tuberculosis (Mtb) infection, less effort has been invested in exploiting the humoral immune system to combat Mtb. Emerging data point to a role for antibodies in microbial control of Mtb, however the precise mechanism(s) of this control remain incompletely understood. Here we took an antibody Fc-engineering approach to determine whether Fc-modifications could improve the ability of antibodies to restrict Mtb, and to define Fc-mediated mechanism(s) antibodies leverage for this restriction. Using an antibody specific to the capsular polysaccharide α-glucan, we engineered a panel of Fc variants to augment or dampen select antibody effector functions, rationally building antibodies with enhanced capacity to promote Mtb restriction in a human whole blood model of infection. Surprisingly, several restrictive Fc-engineered antibodies drove Mtb control in a neutrophil, not monocyte, dependent manner. Using single cell RNA sequencing, we show that an Fc-engineered antibody with restrictive activity promotes neutrophil survival and expression of cell intrinsic antimicrobial programs. These data provide a roadmap for exploiting Fc-engineered antibodies as a novel class of TB therapeutics able to harness the protective functions of neutrophils to achieve disease control.